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Similar effects of intranasal oxytocin administration and acute alcohol consumption on socio-cognitions, emotions and behaviour: Implications for the mechanisms of action

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Oxytocin (OT) plays a critical role in the formation of long lasting social attachments across a range of mammalian species. Raising intracerebral OT levels by intranasal administration of the neuropeptide (inOT) can also have pronounced effects on human sociocognitive functioning. inOT has been associated with increasing altruism, generosity, empathy and trust while decreasing fear, anxiety and stress reactions via neural mechanisms which are yet to be fully elucidated. The observation of the prosocial effects of OT has led to speculation about the role the peptide might play in some psychiatric conditions and debate as to its potential therapeutic uses. Here we note the great similarity in the sociocognitive effects that can be induced by inOT and the effects of acute consumption of modest does of alcohol. We further reflect on how both compounds may act on limbic and prefrontal cortical structures to increase GABAergic transmission, thereby facilitating the release of prepotent responses, that is, more automatic responses which are associated with earlier developmental stages. Copyright © 2015. Published by Elsevier Ltd.
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Mitchell, I. J., Gillespie, S. M., & Abu-Akel, A. (2015). Similar effects of intranasal oxytocin
administration and acute alcohol consumption on socio-cognitions, emotions and behaviour:
Implications for the mechanisms of action. Neuroscience & Biobehavioral Reviews, 55, 98-
106.
This article is the final version of the article accepted
for publication following peer review. The article was
published in the journal Neuroscience and
Biobehavioral Reviews, August 2015.
Title: Similar effects of intranasal oxytocin administration and acute alcohol consumption on
socio-cognitions, emotions and behaviour: Implications for the mechanisms of action
Running title: Oxytocin and alcohol
Authors: Ian J. Mitchell1, Steven M. Gillespie1*, Ahmad Abu-Akel1
Affiliation: 1School of Psychology, University of Birmingham, Birmingham, B152TT, UK.
Corresponding Author: Dr. Steven M. Gillespie, School of Psychology, University of
Birmingham, Birmingham, B15 2TT, UK.
E mail: S.M.Gillespie@bham.ac.uk Tel: +44 121 414 3665
Similar effects of intranasal oxytocin administration and acute alcohol consumption on socio-
cognitions, emotions and behaviour: Implications for the mechanisms of action
1. Introduction
Oxytocin (OT), a neuropeptide hormone released from the posterior pituitary gland, plays
well established roles in childbirth and lactation. More recently, studies of monogamous
voles have led to an understanding of the role that oxytocin plays in the formation of long
lasting social attachments (Carter 1998; Ross et al., 2009; Young & Wang, 2004). Such work
has emphasised how oxytocin released from terminals and dendrites of neurons within the
brain (Ludwig & Leng, 2006) can act on oxytocin receptors expressed by structures such as
the medial nuclei of the amygdala to drive the formation of partner preference (Ferguson et
al., 2001; Young & Wang, 2004; Insel & Young, 2001).
The effects of raising intracerebral oxytocin levels, by intranasal (inOT) administration, on
human social functioning have been extensively researched. Much of this work has involved
studying the effects of inOT on socio-cognitions and emotions. The findings have led to the
general conclusion that raising oxytocin levels is associated with increases in prosocial
behaviours including increased tendencies to behave altruistically, generously and
empathically, and to trust others more (Zak et al., 2007; Barraza & Zak, 2009; Baumgarter et
al., 2008; Kosfeld et al., 2005). This has led to excitement with respect to the possibility of
treating some psychological/psychiatric conditions with the compound (Meyer-Lindenberg et
al., 2011). It should, however, be noted that intranasal oxytocin administration is also
associated with amplifying some aspects of antisocial behaviour, including gloating and
envious responses in relation to competitors (Shamay-Tsoory et al., 2009), and exaggerating
ethnocentric biases (De Dreu et al., 2010, 2011).
One complication relating to interpreting the actions of inOT relates to the degree to which
the peptide can penetrate the blood brain barrier. Systemically administered neuropeptides in
general do not enter the brain with ease. However, the use of inOT procedures may be more
effective than intravenously and other systemic routes. Studies in both animals and humans
have shown that inhalation administered neuropeptides do enter the CSF and can affect
neural activity in structures such as the amygdala without inducing significant peripheral and
hormonal effects (Born, Lange, Kern, McGregor, Bickel, & Fehm, 2002; Striepens et al.
2013).
Much of the detail of the mechanisms by which oxytocin exerts its effects on human social
behaviour is still to be determined. There is currently debate as to whether these changes are
mediated by the neuropeptide exerting specific actions in a selective manner on particular
aspects of social behavior, or whether they result secondarily as a product of more low level
general effects (Churchland & Winkielman, 2012). In this paper we highlight the strong
similarities in the effects elicited by inOT and by acute consumption of modest doses of
alcohol on an array of social-cognitions and emotions, ranging from fear, anxiety and stress,
to aggression and in-group favouritism. We hypothesise that, although the two compounds
work on very different receptors, they nonetheless will induce common effects on GABA
transmission in the prefrontal cortex and limbic structures. Having explored this potentially
common neural mechanism behind the similar socio-affective responses we then explore the
possibility that both drugs act by unmasking modes of acting and thinking that are acquired
earlier in development.
2. Effects of oxytocin and acute alcohol consumption on social-cognitions and behavior
2.1. Fear, anxiety and stress
The potential anxiolytic effects of oxytocin have been inferred from the observation of
reduced anxiety and stress responses in breast feeding/suckling mammals which is
accompanied by increased release of the peptide (UvnasMoberg, 1998). Work with
experimental animals has confirmed this postulated relationship. For example, OT reduces
anxiety when administered directly in to the cerebral ventricles (Windle et al., 1997, Carter et
al., 1998), paraventricular nucleus of the hypothalamus (Blume et al., 2008) and prelimbic
area of the medial prefrontal cortex (Sabihi et al., 2014) of experimental rodents. Sub-
cutaneous injections of OT have also been shown to reduce startle responses in rodents in a
fear-potentiated startle paradigm (Missig et al., 2010), and cause reductions in stress
responses as indicated by attenuated corticosterone (Windle et al., 1997; Mantella et al.,
2004) and ACTH release in rodents and primates (Parker et al., 2005) respectively. It has also
been shown in humans that both plasma and CSF levels of OT significantly negatively
predict trait anxiety scores (Carson et al., 2014).
A series of studies have shown that inOT can similarly reduce fear responses, exert anxiolytic
effects and reduce the release of corticosteroid stress hormones in humans. One of the most
persuasive studies is that by Kirsch et al. (2005), which looked at the acute effects of inOT on
amygdala responses to fear-inducing visual images as shown by fMRI. This work
demonstrated that boosting OT levels in healthy participants reduces both fear responses in
the amygdala itself and the coupling of amygdala activity with that of midbrain structures
involved in autonomic and behavioural aspects of fear responses (see Table 1).
Table 1 about here
Other studies have focused on individuals who suffer from anxiety disorders. In this regard,
Guastella et al. (2009) showed that inOT improves mental representations of the self in
individuals with social anxiety disorder when taken in addition to exposure therapy.
Similarly, Labuschagne et al. (2012) showed in a fMRI study that inOT tempered medial
prefrontal and anterior cingulate responses to negative social cues, including fearful faces, in
patients with generalized social anxiety disorder.
Moreover, inOT reduces cortisol levels in response to acute psychological stressors,
including experimentally induced social rejection (Linnen et al., 2012) and social stress tests,
where an interaction with social support is seen (Heinrichs et al., 2003). These effects,
however, may be attenuated in men who experienced early parental separation (Meinlschmidt
& Heim, 2007). inOT is also reported to reduce the magnitude of cortisol release induced by
physiological stressors such as intense exercise (Cardosa et al., 2013).
The capacity for acute alcohol consumption to reduce anxiety has been known for centuries.
This relationship has been subject to experimental scrutiny in recent years. For example,
Sayette et al. (1992) demonstrated that acute alcohol consumption reduced negative
emotional reactions in social drinkers on a social stressor test. Alcohol can also moderate fear
reactions, and has been shown to reduce amygdala responses in social drinkers to threatening
stimuli (Gilman et al., 2008; Sripada et al., 2011). Similarly, it is thought that individuals who
suffer from social phobia may self-medicate with alcohol (Carrigan & Randall, 2003). These
anxiolytic and fear reducing responses are most likely mediated via an effect of alcohol on
the central and medial nuclei of the amygdala (Pandey, 2006). Alcohol may also be able to
reduce stress effects via an action on the central amygdala (CeA) nuclei. For example, Nie et
al. (2004) showed that alcohol interacts with CRF1 receptors to enhance GABAergic synaptic
transmission in the CeA.
Although acute inOT administration elicits anxiolytic effects, elevated levels of oxytocin may
be associated with prolonged exposure to stressors, especially in early life. For example,
maltreated children show raised urinary OT levels (a marker of cerebral OT levels) as do
adult offenders who experienced early childhood maltreatment (Seltzer et al., 2014; Mitchell
et al., 2013). Similarly, Hoge et al. (2008) showed that plasma oxytocin levels correlated with
higher social anxiety symptoms in patients with Generalized Social Anxiety Disorder
(GSAD). A parallel relationship may occur with alcohol whereby acute consumption
decreases anxiety but chronic consumption and dependence is associated with anxiety
disorders (Schuckit & Hesselbroc, 1994).
2.2. Trust, Generosity and Altruism
A succession of papers has reported that elevated OT levels are associated with increases in
trust, generosity and altruism as measured in social decision making games. For example,
inOT has been associated with the maintenance of trust even after betrayal (Baumgartner et
al., 2008) and irrespective of the tendency to take risks (Kosfeld et al., 2005). Similarly,
Theodoridou et al. (2009) demonstrated that inOT increased the ratings of trustworthiness
and attractiveness of others. Furthermore, inOT can enhance generosity and to a lesser extent,
altruism in one-shot decision making games (Zak et al., 2007).
Similar effects have been reported following acute alcohol consumption. Lynn et al. (1988)
demonstrated that there is a relationship between alcohol consumed and size of tip in
restaurant diners. More formally, Steele et al. (1985) showed that alcohol can dose
dependently make individuals more generous on tasks which involve helping another
complete an unpleasant task. The data suggest that the effect is mediated by alcohol helping
to override inhibiting pressures which act to prevent the expression of generosity.
2.3. Social decision making games
In these games, which include the ultimatum game and the dictator game, participants are
required to carve up either real or imaginary monetary rewards between themselves and in-
groups and out-groups. Both inOT and acute alcohol consumption have been shown to affect
responding behavior on these games by affecting the generosity of responses to out-group
members (Radke & De Bruijn, 2012), and by increasing rejection rates of apparently unfair
offers (Morewedge et al., 2014).
2.4. Morality
Although inOT may increase prosocial behaviours such as trust and generosity, its actions
may be more circumspect than first appears. inOT caused individuals to be more dishonest in
a coin-tossing prediction game in order to benefit fellow group members (Shalvi & De Dreu,
2014). Similarly, acute alcohol consumption can also induce changes in moral behaviour. For
example, Denton and Krebs (1990) demonstrated that alcohol consumption is associated with
transient decreases in moral maturity.
2.5. Facial emotional expression recognition
Several studies have examined the role of OT in the recognition of facial emotional
expressions. Much of this work has contrasted the effects of the neuropeptide on the
recognition of positive versus negative emotions. Several studies have reported that OT
improves the perception of happy faces (Marsh et al., 2010; Schulze et al., 2011). These
findings are supported by the results of a meta-analysis, which concluded that inOT
significantly improves recognition accuracy for happy faces (Shahrestani et al., 2013). In
equivalent experiments involving experimental primates, Parr et al. (2013) showed that inOT
reduced the monkey’s attention to negative facial expressions. However Shahrestani et al.,
(2013) also concluded that fearful faces are also recognised more accurately following inOT,
suggesting that the beneficial effects on recognition may also apply to this negative emotional
expression.
Alcohol, like inOT, affects emotional facial expression recognition. For example, Kano et al.
(2003) showed that a low dose of alcohol significantly improved the recognition of happy
faces but not negative facial emotional expressions. Moreover, others have shown that
alcohol makes sad faces harder to recognise accurately. For example, Kamboj et al. (2013)
showed that alcohol causes sad faces to be classified as neutral, while Craig et al. (2009)
reported that alcohol raised the threshold for the accurate identification of sad faces.
Similarly, Stevens et al. (2006) showed that both social phobic and control participants rated
angry faces as less rejecting following alcohol consumption.
2.6. Risk taking
Although the literature on OT and risk taking in humans is relatively small (for example, see
Kosfeld et al., 2005), there is some impressive literature on this in rodents. This work has
demonstrated that sexual activity and mating induces the release of OT within the
hypothalamic paraventricular nucleus, reduces the level of anxiety and increases risk-taking
behavior in male rats (Waldherr & Neumann, 2007; Kavaliers et al., 2008). Similarly, alcohol
has long been associated with increased risk taking in humans, with recent interests focusing
on the effects of alcohol in increasing the likelihood of risky sexual practices (Cooper, 2002;
Halpern-Felsher et al., 1996).
2.7. Analgesia
The potential analgesic effects of OT are reviewed by Uvnas Moberg (1998). Daily injections
of OT for 5 days increased the withdrawal latency to a hot noxious stimulus in a tail flick test
(Agren et al., 1995). Furthermore, Kavaliers et al. (2006) showed that OT knockout mice
show an attenuation of the analgesic response, as shown by decreased latency in foot
withdrawal in a hot-plate test, which is normally elicited by exposure to an infected
conspecific.
The analgesic effects of alcohol have been known since ancient Greek times (Rosso, 2012).
Experiments have shown that acute alcohol administration results in a transient lowering of
the sensitivity to painful electric shocks (Stewart, 1995) and a significant increase in pain
tolerance but not pain threshold (Perrino et al., 2008).
2.8. Aggression
Although OT is associated with prosocial behaviours, there are nonetheless positive
relationships between OT and aggressiveness under particular circumstances. This may
reflect the role of OT in parenting and maternal aggression (Debiec, 2005). However, inOT
also increases the probability of aggression towards an intimate partner as self-disclosed by
participants following a provocation task (De Wall et al., 2014). This effect, however, was
limited to participants with high trait physical aggressiveness.
An association between the expression of aggressive behaviours and alcohol is well
established (e.g., Giancola & Parrott, 2008; Hoaken & Pihl, 2000). However, Giancola
(2002) demonstrated that, like inOT, the effect of alcohol on increasing aggressive responses
in the Taylor Aggression Paradigm, where electric shocks are administered to a fictitious
opponent during a competitive task, is limited to individuals with high dispositional
aggressivity.
Related observations of how the effects of inOT are dependent on both personality traits and
context have been reviewed by others (Bartz, Zaki, Bolger, & Ochsner, 2011; Quintana,
Alvares, Hickie, & Guastella, 2015). These reports emphasize how personality and individual
differences along with situational factors can markedly influence the cognitive, affective and
behavioural responses to inOT.
2.9. Reward
The role that OT plays in driving the formation of attachments between conspecifics has led
to the hypothesis that OT can act on the brain’s reward circuits by encouraging the release of
dopamine by ventral tegmental area (VTA) neurons into the nucleus accumbens. This
hypothesis has been supported by Liu and Wang (2003) who showed that interactions of
dopamine and oxytocin systems in the striatum are needed for forming and maintaining
attachment bonds. Further support is provided by the observation that OT dose-dependently
excites dopamine neurons in the VTA (Tang et al., 2014), and acts as a reinforcer, like other
drugs and natural rewards, under both solitary and social conditions (Kent et al., 2013).
Similar observations have also been made with respect to alcohol. For example, Xiao and Ye
(2008) showed that alcohol boosts activity in VTA dopamine neurons by an action on local
GABAergic mechanisms. Furthermore, Gilman et al. (2008) showed in an fMRI study that
alcohol strongly activated striatal reward circuits, with the level of activation correlating with
the levels of self-rated intoxication.
2.10. Empathy/Theory of Mind (ToM)/Eye gaze
Understanding the role of OT in mediating empathic responses is made difficult by the
complexity of the empathy concept in itself. There is general agreement that empathy can be
subdivided into affective empathy, or emotional contagion, and cognitive empathy, which
includes perspective taking and ToM (Bernhardt & Singer, 2012; Decety, 2011; Shamay-
Tsoory, 2011). Shamay-Tsoory et al. (2009) have elegantly demonstrated that these two
different components of empathy are mediated by dissociable neuronal networks.
Furthermore, it appears that affective empathy appears earlier in development than cognitive
empathy (Shamay-Tsoory et al. 2009).
There are reports of inOT increasing empathic sensitivity. For example, Krueger et al. (2013)
reported that inOT increased the perception of harm for victims. Moreover, Shamay-Tsoory
et al. (2013) showed that inOT increased estimates of how much pain a member of an ethnic
out-group was experiencing as a product of an accident. Hurlemann et al. (2010) similarly
reported that inOT potentiated emotional empathic responses to both positive and negative
valence stimuli. However, no equivalent effects were seen for cognitive empathy.
By contrast, Domes et al. (2007) showed that inOT improved performance on the Reading the
Mind in the Eyes Test, a test of ToM which necessitates inferring an individual’s emotions on
the basis of images of the eye region of their face. inOT may also exert an influence over
emotion recognition by affecting eye scan paths. Both Domes et al. (2013) and Guastella et
al. (2008) have shown that inOT increases the number of fixations and total gaze time toward
the eye region of faces, that is, the facial region that is particularly rich in emotional cues.
There are surprisingly few articles reporting the effects of acute alcohol consumption on
empathy. However, one study has reported that alcohol increases affective empathy, whereby
acute alcohol consumption increases the contagion of true smiles (Duchenne smiles),
especially in males interacting with females (Fairbairn & Sayette, 2014).
2.11. In-group favouritism/out-group derogation and in-group conformity
Despite the predominance of articles on the pro-social effects of OT, there are nonetheless
some reports of it generating negative social cognitions. For example, Shamay-Tsoory et al.
(2009) reported that inOT increases envy and gloating in competitive game situations. In a
similar vein, De Dreu and colleagues (2010, 2011) have reported that inOT promotes
parochial altruism, that is, a tendency to support an in-group at the expense of an out-group.
De Dreu et al. (2011) showed that inOT was associated with a tendency to promote in-group
trust and cooperation, alongside defensive aggression toward competing out-groups.
Moreover, Sheng et al. (2013) reported that inOT enhances an EEG correlate of empathic
responding to images of ethnic in-group faces, but not out-group faces, feeling pain. Stallen
et al. (2012) also showed that inOT enhanced the tendency for individuals to express the
same opinions and judgments as members of their in-group.
Equivalent effects have been reported following acute alcohol consumption. For example,
Mitchell et al. (2015) showed that drinking modest doses of alcohol resulted in Caucasian
participants judging White faces to be more attractive than when sober. However, this effect
was not seen when the participants judged black faces and is thus indicative of alcohol
promoting in-group favouritism. Moreover, Kirchner et al. (2006) showed that acute alcohol
consumption increases the co-ordination of verbal and non-verbal behaviours and self-
reported bonding between in-group members. Furthermore, Sayette et al. (2012) showed in a
large scale study with over 700 participants, that alcohol facilitated bonding in social groups,
promoted smiling and reduced individual level behaviours associated with negative affect.
2.12. Subjective effects of inOT and acute alcohol consumption
Although a myriad of socioaffective effects have been described following inOT, the
procedure is not generally associated with marked subjective changes in mood (Kirkpartrick
et al., 2014; MacDonald et al. 2011). With the typically used single dose of OT, in the range
of 20-40 IU, effects of euphoria, light headedness and drowsiness have only occasionally
been reported and participants are only rarely able to reliably determine whether they
received inOT or placebo (MacDonald et al. 2011). By contrast, alcohol clearly has the
capacity to induce marked changes in mood. It should be noted, however, that low to
moderate doses of alcohol do not necessarily induce subjective changes in mood. Indeed,
double blind laboratory based experiments with low to moderate doses of alcohol are
frequently conducted where the participants are unaware of whether they consumed the
alcoholic drink or placebo (Kirchner et al., 2006; Sayette et al., 2012; Sripada et al., 2011;
Steele et al., 1985).
3. Potential common neurobiological mechanisms underlying the effects of inOT
and acute alcohol consumption and therapeutic implications
This extensive list of similar socio-cognitive responses resulting from the administration of
inOT and acute alcohol consumption implies that the two drugs are ultimately acting on
common neural circuits. Thus, although the two ligands act at different receptors they may
nonetheless exert equivalent actions on prefrontal and limbic circuits.
Alcohol exerts its primary pharmacological action by acting synergistically with GABA,
primarily at variants of the GABA-A receptor complex which contain a delta subunit
(Roberto et al., 2003; Akk & Steinbach, 2003). Most of the effects of alcohol on social
behaviour are thus thought to reflect the ligand modifying GABA transmission in: the
amygdala to reduce anxiety, the VTA/nucleus accumbens to elicit a sense of reward, and
parts of the prefrontal cortex. Many of the socio-affective actions of oxytocin may likewise
reflect modifications of GABAergic transmission. Indeed, Viviani et al. (2010) have shown
using in vitro techniques that oxytocin acts presynaptically to induce a massive release of
GABA from neurons in the central amygdala nuclei while benzodiazepines induce similar
effects at a circuit level by acting synergistically with GABA post-synaptically (see Figure 1).
Consequently, both inOT and acute alcohol consumption would result in an equivalent
increase in GABAergic mediated inhibition of the circuit. Similarly, Bulbul et al. (2011)
demonstrated that some of the anxiolytic effects of OT are mediated via its actions on
GABA-A receptors in the hypothalamus and Owen et al. (2013) has argued that analogous
OT/GABA interactions operate in the hippocampus to inhibit pyramidal neurons.
Figure 1 about here
If this model of oxytocin functioning is correct, it follows that the potential therapeutic
actions of OT could be mimicked by alcohol, or by any manipulation that boosts GABA-A
receptor mediated function, including administration of benzodiazepines. Tentative support
for this claim can be found. Preliminary evidence suggests that inOT can ameliorate the
symptoms of autism and increase socio-cognitive functioning in affected individuals (Andari
et al., 2010; Hollander et al., 2007, 2003; Guastella et al., 2010). Equally Han and colleagues
have shown that low, non-sedative and non-anxiolytic, doses of benzodiazepines improve
deficits in social interaction in a mouse model of idiopathic autism (Han et al., 2014). The
hyper-connectiveness model of autism (see Courchesne et al., 2007) speculates that aberrant
functioning in autism results from early brain overgrowth. This overgrowth is thought to
result in an excess of local cortical interactions which impede the functional interactions
between more distant brain sites. Pharmacological manipulations which increase GABA
transmission and so reduce the activity of these local cortical systems would consequently be
expected to have a therapeutic effect.
4. Effects of acute alcohol consumption and inOT on prepotent responses and
socio-affective responses seen in children
Although alcohol exerts its primary pharmacological action by boosting GABA-mediated
inhibition, its effects on socio-affective behaviours are typically attributed to a process of
disinhibition. For instance, alcohol can be seen as impeding the activity of high level
prefrontal cortical regions and the resultant compromised executive function allows the
expression of an otherwise suppressed behavioural response. Alcohol induced release of
prepotent responses can, for example, be seen in Stroop tasks (Marinkovic et al., 2012; Rose
& Duka 2008), n-back working memory tasks (Casbon et al., 2003) and go/no-go tasks (Rose
& Duka, 2008).
The release of prepotent responses following alcohol consumption may lead to socio-
cognitive behaviours that are similar to those observed among young children at early stages
of prefrontal development. Executive functioning is known to be limited in infants, with
children around the age of 4-5 showing difficulties in inhibiting prepotent responses (Livesey
& Morgan,1991; Kerr & Zelazo, 2004). However, adolescents still perform more poorly than
young adults on Stroop tests (Vijayakumar et al., 2014, Veroude et al., 2013). This gradual
and protracted development of executive functioning is assumed to reflect the prolonged
maturation of the prefrontal cortex which continues into adulthood. This slow process is
characterised by a shift in reliance on ventromedial areas of the prefrontal cortex for
resolving cognitive interference to structures which lie more dorsolaterally. This mirrors the
shift from the ready expression of emotional and instinctual behaviors to more controlled and
abstract responses (Fuster, 2002).
Following on from this it can be argued that acute alcohol consumption, and by analogy
inOT, will encourage the release of prepotent responses, that is, responses that would be more
typical of those made at an earlier developmental stage. A considerable array of evidence
supports this position as follows.
4.1. Trust
There is some evidence to suggest that young children intrinsically trust others prior to
developing a sense of mistrust (See Table 2). Vanderbilt et al. (2011), for example, showed
that three year old children accept advice from reliable and unreliable helpers in an
experimental game, whereas 5 year olds showed selective trust and would only take advice
from reliable helpers. Similarly, Heyman et al. (2013) showed that 3 year old children have
trouble ignoring misleading advice if it appears to have been intentionally offered by others.
Thus, inOT could be seen as enabling the release of the default condition of trusting.
Table 2 about here
4.2. Altruism
Warneken and Tomasello (2008, 2009) argue that although altruism is rare in non-humans it
is present in very young children. For example, it has been shown that 18 month old children
readily help others to achieve their goals. This altruistic behaviour appears to be intrinsically
driven and can be disrupted if extrinsic rewards are given in an attempt to reinforce the pro-
social behaviour. Similarly, Harbaugh et al. (2000) showed that children around the age of 6
years respond differently to 12 year old children and adults in a public goods game.
Participants of all ages show initial altruistic behaviour but this is only maintained in younger
children. This parallels the inOT maintenance of trust following betrayal as shown by
Baumgartner et al. (2008).
4.3. Gloating/spite
Fehr et al. (2013) reported that spitefulness decreases with increasing age amongst children
aged from 8-17 years. This effect matches the increase in envy and gloating that can be
elicited by inOT (Shamay-Tsoory et al., 2009).
4.4. In-group favoritism
In-group love can be seen in preschool children (Buttelmann & Boehm, 2014) and can drive
in-group biases. However, out-group hate only appears in children over the age of six years.
Similarly, Inguglia and Musso (2013) studied reactions to national out-groups in Italian
children. In-group favouritism was seen in children from the age of six, whereas derogation
of a national out-group was only seen in older children. These observations are equivalent to
those of De Dreu and colleagues who showed that inOT promotes in-group favouritism
without necessarily inducing large out-group derogation effects (De Dreu et al., 2010). (See
table 1)
4.5. Empathy and sympathy
Roth-Hanania et al. (2011) showed that children as young as 24 months old can show
empathy for the distress of another. Furthermore, Decety and Michalska (2010) imaged the
brain mechanisms that respond to seeing pain intentionally inflicted on another individual.
Neural activity shifted from medial prefrontal structures, which predominated in the brains of
7 year olds, to lateral prefrontal areas in adults. This may underlie a move from visceral
responses to the affective stimuli to more abstract cognitive responses and so parallel the
effect of inOT in potentiating emotional but not cognitive empathy (Hurlemann et al., 2010).
4.6. Happy facial expressions
Gao and Maurer (2010) demonstrated that children are as sensitive as adults to facial
expressions of happiness from the age of 5 years. However, sensitivity to other facial
emotional expressions develops gradually up to the age of 10 years with sensitivity to anger
and sadness developing last. This would correspond to the observed effects of inOT on
preferentially boosting the recognition of happy facial expressions relative to negative ones
(Marsh et al., 2010; Schulze et al., 2011; Shahrestani et al., 2013).
5. Conclusion
The similarity in behavioural/cognitive/emotional effects induced by inOT and alcohol, taken
together with their common effects on GABAergic transmission in identified neural circuits,
implies that the two compounds act in similar ways. A plausible model to account for their
social effects would be the removal of inhibitory brakes which normally act to suppress the
expression of response tendencies that are characteristic of earlier developmental stages.
From this it would be predicted that both inOT and alcohol would exert greater effects on
inhibiting circuits in the dorsolateral prefrontal cortex than the more primitive ventromedial
cortex.
This analysis also implies that any therapeutic effects induced by inOT could potentially be
elicited by other pharmacological manipulations which boost GABAergic transmission in
specific neural circuits. Such manipulations would include the administration of
benzodiazepines. Indeed, as noted above, low doses of benzodiazepines have recently been
shown to be beneficial in an animal model of autism (Han et al., 2014). However, given the
addictive and dependency issues surrounding both alcohol and benzodiazepines, their long
term use in treating chronic neuropsychiatric conditions would have to be pursued with
extreme caution. Against this background it is chastening to note how little is known about
the chronic effects of inOT.
The conclusion that oxytocin is exerting many of its socio-cognitive effects by suppressing
the action of prefrontal and limbic cortical circuits may at first sight seem surprising.
However, few psychoactive drugs exert their actions by boosting neuronal activity in the
sophisticated ways needed to encode for trust, generosity, empathy etc. Psychoactive drugs
are far more likely to elicit effects by reducing unwanted neural activity. Exceptions would
include drugs that boost monoamine transmission such as dopaminergic agents used to treat
the symptoms of Parkinson’s disease. But even here, the drugs are most likely enabling
normal cortical functioning to resume by reducing the interference from abnormally
discharging basal ganglia structures (Mitchell et al., 1989). If this conjecture is correct, then it
would appear that inOT may act by unmasking your inner child.
6. References
Agren, G., Lundeberg, T., Uvna¨s-Moberg, K., & Sato, A. (1995) The oxytocin antagonist 1-
deamino-2-D-Tyr (Oet)-4-Thr-8-Orn oxytocin reverses the increase in the withdrawal
response latency to thermal, but not mechanical nociceptive stimuli following oxytocin
administration or massage-like stroking in rats. Neuroscience Letters, 187, 4952.
Akk, G., & Steinbach, J. H. (2003). Low doses of ethanol and a neuroactive steroid positively
interact to modulate rat GABAA receptor function. The Journal of Physiology, 546, 641-
646.
Andari, E., Duhamel, J. R., Zalla, T., Herbrecht, E., Leboyer, M., & Sirigu, A. (2010).
Promoting social behavior with oxytocin in high-functioning autism spectrum
disorders. Proceedings of the National Academy of Sciences, 107, 4389-4394.
Barraza, J. A., & Zak, P. J. (2009). Empathy toward strangers triggers oxytocin release and
subsequent generosity. Annals of the New York Academy of Sciences, 1167, 182-189.
Bartz, J. A., Zaki, J., Bolger, N., & Ochsner, K. N. (2011). Social effects of oxytocin in
humans: Context and person matter. Trends in Cognitive Sciences, 15, 301-309.
Baumgartner, T., Heinrichs, M., Vonlanthen, A., Fischbacher, U., & Fehr, E. (2008).
Oxytocin shapes the neural circuitry of trust and trust adaptation in humans. Neuron, 58,
639-650.
Bernhardt B. C. & Singer, T. (2012). The neural basis of empathy. Annual Review of
Neuroscience, 35, 1-23.
Blume, A., Bosch, O. J., Miklos, S., Torner, L., Wales, L., Waldherr, M., & Neumann, I. D.
(2008). Oxytocin reduces anxiety via ERK1/2 activation: local effect within the rat
hypothalamic paraventricular nucleus. European Journal of Neuroscience, 27, 1947-
1956.
Born, J., Lange, T., Kern, W., McGregor, G. P., Bickel, U., & Fehm, H. L. (2002). Sniffing
neuropeptides: A transnasal approach to the human brain. Nature Neuroscience, 5, 514-
516.
Bülbül, M., Babygirija, R., Cerjak, D., Yoshimoto, S., Ludwig, K., & Takahashi, T. (2011).
Hypothalamic oxytocin attenuates CRF expression via GABA A receptors in rats. Brain
Research, 1387, 39-45.
Buttelmann, D., & Böhm, R. (2014). The ontogeny of the motivation that underlies in-group
bias. Psychological Science. doi: 10.1177/0956797613516802
Cardoso, C., Ellenbogen, M. A., Orlando, M. A., Bacon, S. L., & Joober, R. (2013).
Intranasal oxytocin attenuates the cortisol response to physical stress: a doseresponse
study. Psychoneuroendocrinology, 38, 399-407.
Carrigan, M. H., & Randall, C. L. (2003). Self-medication in social phobia: a review of the
alcohol literature. Addictive Behaviors, 28, 269-284.
Carson, D. S., Berquist, S. W., Trujillo, T. H., Garner, J. P., Hannah, S. L., Hyde, S. A., ... &
Parker, K. J. (2014). Cerebrospinal fluid and plasma oxytocin concentrations are
positively correlated and negatively predict anxiety in children. Molecular Psychiatry.
doi: 10.1038/mp.2014.132
Carter, C. S. (1998). Neuroendocrine perspectives on social attachment and
love. Psychoneuroendocrinology, 23, 779-818.
Casbon, T. S., Curtin, J. J., Lang, A. R., & Patrick, C. J. (2003). Deleterious effects of alcohol
intoxication: diminished cognitive control and its behavioral consequences. Journal of
Abnormal Psychology, 112, 476-.
Churchland, P. S., & Winkielman, P. (2012). Modulating social behavior with oxytocin: how
does it work? What does it mean? Hormones and Behavior, 61, 392-399
Cooper, M. L. (2002). Alcohol use and risky sexual behavior among college students and
youth: Evaluating the evidence. Journal of Studies on Alcohol and Drugs, 14, 101-117.
Courchesne, E., Pierce, K., Schumann, C. M., Redcay, E., Buckwalter, J. A., Kennedy, D. P.,
& Morgan, J. (2007). Mapping early brain development in autism. Neuron, 56, 399-413.
Craig, L. C., Attwood, A. S., Benton, C. P., Penton-Voak, I. S., & Munafo, M. R. (2009).
Effects of acute alcohol consumption and alcohol expectancy on processing of perceptual
cues of emotional expression. Journal of Psychopharmacology, 23, 258-265.
Dębiec, J. (2005). Peptides of love and fear: vasopressin and oxytocin modulate the
integration of information in the amygdala. Bioessays, 27, 869-873.
Decety, J. (2011). Dissecting the neural mechanisms mediating empathy. Emotion Review 3,
92108.
Decety, J., & Michalska, K. J. (2010). Neurodevelopmental changes in the circuits underlying
empathy and sympathy from childhood to adulthood. Developmental Science, 13, 886-
899.
De Dreu, C. K., Greer, L. L., Handgraaf, M. J., Shalvi, S., Van Kleef, G. A., Baas, M., ... &
Feith, S. W. (2010). The neuropeptide oxytocin regulates parochial altruism in intergroup
conflict among humans. Science, 328, 1408-1411.
De Dreu, C. K., Greer, L. L., Van Kleef, G. A., Shalvi, S., & Handgraaf, M. J. (2011).
Oxytocin promotes human ethnocentrism. Proceedings of the National Academy of
Sciences, 108, 1262-1266.
Denton, K., & Krebs, D. (1990). From the scene to the crime: The effect of alcohol and social
context on moral judgment. Journal of Personality and Social Psychology, 59, 242-248.
DeWall, C. N., Gillath, O., Pressman, S. D., Black, L. L., Bartz, J. A., Moskovitz, J., &
Stetler, D. A. (2014). When the love hormone leads to violence oxytocin increases
intimate partner violence inclinations among high trait aggressive people. Social
Psychological and Personality Science. doi: 10.1177/1948550613516876.
Domes, G., Heinrichs, M., Michel, A., Berger, C., & Herpertz, S. C. (2007). Oxytocin
improves “mind-reading” in humans. Biological Psychiatry, 61, 731-733.
Domes, G., Steiner, A., Porges, S. W., & Heinrichs, M. (2013). Oxytocin differentially
modulates eye gaze to naturalistic social signals of happiness and
anger. Psychoneuroendocrinology, 38, 1198-1202.
Fairbairn, C. E., & Sayette, M. A. (2014). A social-attributional analysis of alcohol
response. Psychological Bulletin, 140, 1361-1382.
Fehr, E., Glätzle-Rützler, D., & Sutter, M. (2013). The development of egalitarianism,
altruism, spite and parochialism in childhood and adolescence. European Economic
Review, 64, 369-383.
Ferguson, J. N., Aldag, J. M., Insel, T. R., & Young, L. J. (2001). Oxytocin in the medial
amygdala is essential for social recognition in the mouse. The Journal of
Neuroscience, 21, 8278-8285.
Fuster, J. M. (2002). Frontal lobe and cognitive development. Journal of
Neurocytology, 31(3-5), 373-385.
Gao, X., & Maurer, D. (2010). A happy story: Developmental changes in children’s
sensitivity to facial expressions of varying intensities. Journal of Experimental Child
Psychology, 107, 67-86.
Giancola, P. R. (2002). Alcohol-related aggression in men and women: The influence of
dispositional aggressivity. Journal of Studies on Alcohol and Drugs, 63, 696-.
Giancola, P. R., & Parrott, D. J. (2008). Further evidence for the validity of the Taylor
aggression paradigm. Aggressive Behavior, 34, 214-229.
Gilman, J. M., Ramchandani, V. A., Davis, M. B., Bjork, J. M., & Hommer, D. W. (2008).
Why we like to drink: a functional magnetic resonance imaging study of the rewarding
and anxiolytic effects of alcohol. The Journal of Neuroscience, 28, 4583-4591.
Guastella, A. J., Carson, D. S., Dadds, M. R., Mitchell, P. B., & Cox, R. E. (2009). Does
oxytocin influence the early detection of angry and happy faces?
Psychoneuroendocrinology, 34, 220-225.
Guastella, A. J., Einfeld, S. L., Gray, K. M., Rinehart, N. J., Tonge, B. J., Lambert, T. J., &
Hickie, I. B. (2010). Intranasal oxytocin improves emotion recognition for youth with
autism spectrum disorders. Biological Psychiatry, 67, 692-694.
Guastella, A. J., Howard, A. L., Dadds, M. R., Mitchell, P., & Carson, D. S. (2009). A
randomized controlled trial of intranasal oxytocin as an adjunct to exposure therapy for
social anxiety disorder. Psychoneuroendocrinology, 34, 917-923.
Guastella, A. J., Mitchell, P. B., & Dadds, M. R. (2008). Oxytocin increases gaze to the eye
region of human faces. Biological Psychiatry, 63, 3-5.
Halpern-Felsher, B. L., Millstein, S. G., & Ellen, J. M. (1996). Relationship of alcohol use
and risky sexual behavior: a review and analysis of findings. Journal of Adolescent
Health, 19, 331-336.
Han, S., Tai, C., Jones, C. J., Scheuer, T., & Catterall, W. A. (2014). Enhancement of
inhibitory neurotransmission by GABAA receptors having α2,3-subunits ameliorates
behavioral deficits in a mouse model of autism. Neuron, 81, 1282-1289.
Harbaugh, W. T., & Krause, K. (2000). Children's altruism in public good and dictator
experiments. Economic Inquiry, 38, 95-109.
Heinrichs, M., Baumgartner, T., Kirschbaum, C., & Ehlert, U. (2003). Social support and
oxytocin interact to suppress cortisol and subjective responses to psychosocial
stress. Biological Psychiatry, 54, 1389-1398.
Heyman, G. D., Sritanyaratana, L., & Vanderbilt, K. E. (2013). Young children's trust in
overtly misleading advice. Cognitive Science, 37, 646-667.
Hoaken, P. N.S., & Pihl, R. O. (2000). The effects of alcohol intoxication on aggressive
responses in men and women. Alcohol and Alcoholism, 35, 471-477.
Hoge, E. A., Pollack, M. H., Kaufman, R. E., Zak, P. J., & Simon, N. M. (2008). Oxytocin
levels in social anxiety disorder. CNS Neuroscience & Therapeutics, 14, 165-170.
Hollander, E., Bartz, J., Chaplin, W., Phillips, A., Sumner, J., Soorya, L., ... & Wasserman, S.
(2007). Oxytocin increases retention of social cognition in autism. Biological
Psychiatry, 61, 498-503.
Hollander, E., Novotny, S., Hanratty, M., Yaffe, R., DeCaria, C. M., Aronowitz, B. R., &
Mosovich, S. (2003). Oxytocin infusion reduces repetitive behaviors in adults with
autistic and Asperger's disorders. Neuropsychopharmacology, 28, 193-198.
Hurlemann, R., Patin, A., Onur, O. A., Cohen, M. X., Baumgartner, T., Metzler, S., ... &
Kendrick, K. M. (2010). Oxytocin enhances amygdala-dependent, socially reinforced
learning and emotional empathy in humans. The Journal of Neuroscience, 30, 4999-
5007.
Inguglia, C., & Musso, P. (2013). In-group favouritism and out-group derogation towards
national groups: Age-related differences among Italian school children. International
Journal of Intercultural Relations, 37, 385-390.
Insel, T. R., & Young, L. J. (2001). The neurobiology of attachment. Nature Reviews
Neuroscience, 2, 129-136.
Kano, M., Gyoba, J., Kamachi, M., Mochizuki, H., Hongo, M., & Yanai, K. (2003). Low
doses of alcohol have a selective effect on the recognition of happy facial
expressions. Human Psychopharmacology: Clinical and Experimental, 18, 131-139.
Kamboj, S. K., Joye, A., Bisby, J. A., Das, R. K., Platt, B., & Curran, H. V. (2013).
Processing of facial affect in social drinkers: a doseresponse study of alcohol using
dynamic emotion expressions. Psychopharmacology, 227, 31-39.
Kavaliers, M., Choleris, E., Ågmo, A., Braun, W. J., Colwell, D. D., Muglia, L. J., ... & Pfaff,
D. W. (2006). Inadvertent social information and the avoidance of parasitized male mice:
a role for oxytocin. Proceedings of the National Academy of Sciences of the United
States of America, 103, 4293-4298.
Kavaliers, M., Devidze, N., Choleris, E., Fudge, M., Gustafsson, J. Å., Korach, K. S., ... &
Ogawa, S. (2008). Estrogen receptors α and β mediate different aspects of the facilitatory
effects of female cues on male risk taking. Psychoneuroendocrinology, 33, 634-642.
Kent, K., Arientyl, V., Khachatryan, M. M., & Wood, R. I. (2013). Oxytocin induces a
conditioned social preference in female mice. Journal of Neuroendocrinology, 25, 803-
810.
Kerr, A., & Zelazo, P. D. (2004). Development of “hot” executive function: The children’s
gambling task. Brain and Cognition, 55, 148-157.
Kirchner, T. R., Sayette, M. A., Cohn, J. F., Moreland, R. L., & Levine, J. M. (2006). Effects
of alcohol on group formation among male social drinkers. Journal of Studies on Alcohol
and Drugs, 67, 785.
Kirkpatrick, M. G., Lee, R., Wardle, M. C., Jacob, S., & de Wit, H. (2014). Effects of
MDMA and intranasal oxytocin on social and emotional processing.
Neuropsychopharmacology, 39, 1654-1663.
Kirsch, P., Esslinger, C., Chen, Q., Mier, D., Lis, S., Siddhanti, S., ... & Meyer-Lindenberg,
A. (2005). Oxytocin modulates neural circuitry for social cognition and fear in
humans. The Journal of Neuroscience, 25, 11489-11493.
Kosfeld, M., Heinrichs, M., Zak, P. J., Fischbacher, U., & Fehr, E. (2005). Oxytocin
increases trust in humans. Nature, 435, 673-676.
Krueger, F., Parasuraman, R., Moody, L., Twieg, P., de Visser, E., McCabe, K., ... & Lee, M.
R. (2013). Oxytocin selectively increases perceptions of harm for victims but not the
desire to punish offenders of criminal offenses. Social Cognitive and Affective
Neuroscience, 8, 494-498.
Labuschagne, I., Phan, K. L., Wood, A., Angstadt, M., Chua, P., Heinrichs, M., ... & Nathan,
P. J. (2012). Medial frontal hyperactivity to sad faces in generalized social anxiety
disorder and modulation by oxytocin. The International Journal of
Neuropsychopharmacology, 15, 883-896.
Linnen, A. M., Ellenbogen, M. A., Cardoso, C., & Joober, R. (2012). Intranasal oxytocin and
salivary cortisol concentrations during social rejection in university students. Stress, 15,
393-402.
Liu, Y., & Wang, Z. X. (2003). Nucleus accumbens oxytocin and dopamine interact to
regulate pair bond formation in female prairie voles. Neuroscience, 121(3), 537-544.
Livesey, D. J., & Morgan, G. A. (1991). The development of response inhibition in 4and
5yearold children. Australian Journal of Psychology, 43, 133-137.
Ludwig, M., & Leng, G. (2006). Dendritic peptide release and peptide-dependent
behaviours. Nature Reviews Neuroscience, 7, 126-136.
Lynn, M. (1988). The effects of alcohol consumption on restaurant tipping. Personality and
Social Psychology Bulletin, 14, 87-91.
MacDonald, E., Dadds, M. R., Brennan, J. L., Williams, K., Levy, F., & Cauchi, A. J. (2011).
A review of safety, side-effects and subjective reactions to intranasal oxytocin in human
research. Psychoneuroendocrinology, 36, 1114-1126.
Mantella, R. C., Vollmer, R. R., Rinaman, L., Li, X., & Amico, J. A. (2004). Enhanced
corticosterone concentrations and attenuated Fos expression in the medial amygdala of
female oxytocin knockout mice exposed to psychogenic stress. American Journal of
Physiology-Regulatory, Integrative and Comparative Physiology, 287, R1494-R1504.
Marinkovic, K., Rickenbacher, E., Azma, S., & Artsy, E. (2012). Acute alcohol intoxication
impairs topdown regulation of stroop incongruity as revealed by blood oxygen
leveldependent functional magnetic resonance imaging. Human Brain Mapping, 33,
319-333.
Marsh, A. A., Henry, H. Y., Pine, D. S., & Blair, R. J. R. (2010). Oxytocin improves specific
recognition of positive facial expressions. Psychopharmacology, 209, 225-232.
Meinlschmidt, G., & Heim, C. (2007). Sensitivity to intranasal oxytocin in adult men with
early parental separation. Biological Psychiatry, 61, 1109-1111.
Meyer-Lindenberg, A., Domes, G., Kirsch, P., & Heinrichs, M. (2011). Oxytocin and
vasopressin in the human brain: social neuropeptides for translational medicine. Nature
Reviews Neuroscience, 12, 524-538.
Missig, G., Ayers, L. W., Schulkin, J., & Rosen, J. B. (2010). Oxytocin reduces background
anxiety in a fear-potentiated startle paradigm. Neuropsychopharmacology, 35, 2607-
2616.
Mitchell, I. J., Clarke, C. E., Boyce, S., Robertson, R. G., Peggs, D., Sambrook, M. A., &
Crossman, A. R. (1989). Neural mechanisms underlying parkinsonian symptoms based
upon regional uptake of 2-deoxyglucose in monkeys exposed to 1-methyl-4-phenyl-1, 2,
3, 6-tetrahydropyridine.Neuroscience, 32, 213-226.
Mitchell, I. J., Gillespie, S. M., Leverton, M., Llewellyn, V., Neale, E., & Stevenson, I.
(2015). Acute alcohol consumption and secondary psychopathic traits increase ratings of
the attractiveness and health of ethnic ingroup faces but not outgroup faces. Frontiers in
Psychiatry, 6. doi: 10.3389/fpsyt.2015.00025
Mitchell, I. J., Rutherford, V., Wrinch, K. A. J., & Egan, V. (2008). Paradoxical effects of
alcohol intake in a convivial social setting on attitudes to violence. Addiction Research &
Theory, 16, 503-513.
Mitchell, I. J., Smid, W., Troelstra, J., Wever, E., Ziegler, T. E., & Beech, A. R. (2013).
Psychopathic characteristics are related to high basal urinary oxytocin levels in male
forensic patients. Journal of Forensic Psychiatry & Psychology, 24, 309-318.
Morewedge, C. K., Krishnamurti, T., & Ariely, D. (2014). Focused on fairness: Alcohol
intoxication increases the costly rejection of inequitable rewards. Journal of
Experimental Social Psychology, 50, 15-20.
Nie, Z., Schweitzer, P., Roberts, A. J., Madamba, S. G., Moore, S. D., & Siggins, G. R.
(2004). Ethanol augments GABAergic transmission in the central amygdala via CRF1
receptors. Science, 303, 1512-1514.
Owen, S. F., Tuncdemir, S. N., Bader, P. L., Tirko, N. N., Fishell, G., & Tsien, R. W. (2013).
Oxytocin enhances hippocampal spike transmission by modulating fast-spiking
interneurons. Nature, 500, 458-462.
Pandey, S. C., Zhang, H., Roy, A., & Misra, K. (2006). Central and medial amygdaloid brain-
derived neurotrophic factor signaling plays a critical role in alcohol-drinking and
anxiety-like behaviors. The Journal of Neuroscience, 26, 8320-8331.
Parker, K. J., Buckmaster, C. L., Schatzberg, A. F., & Lyons, D. M. (2005). Intranasal
oxytocin administration attenuates the ACTH stress response in
monkeys. Psychoneuroendocrinology, 30, 924-929.
Parr, L. A., Modi, M., Siebert, E., & Young, L. J. (2013). Intranasal oxytocin selectively
attenuates rhesus monkeys’ attention to negative facial expressions.
Psychoneuroendocrinology, 38, 1748-1756.
Perrino, A. C., Ralevski, E., Acampora, G., Edgecombe, J., Limoncelli, D., & Petrakis, I. L.
(2008). Ethanol and pain sensitivity: effects in healthy subjects using an acute pain
paradigm. Alcoholism: Clinical and Experimental Research, 32, 952-958.
Petersson, M., Hulting, A. L., & Uvnäs-Moberg, K. (1999). Oxytocin causes a sustained
decrease in plasma levels of corticosterone in rats. Neuroscience letters, 264, 41-44.
Quintana, D. S., Alvares, G. A., Hickie, I. B., & Guastella, A. J. (2014). Do delivery routes of
intranasally administered oxytocin account for observed effects on social cognition and
behavior? A two-level model. Neuroscience & Biobehavioral Reviews, 49, 182-192.
Radke, S., & De Bruijn, E. R. (2012). The other side of the coin: oxytocin decreases the
adherence to fairness norms. Frontiers in Human Neuroscience, 6, 193, 1-7.
Roberto, M., Madamba, S. G., Moore, S. D., Tallent, M. K., & Siggins, G. R. (2003). Ethanol
increases GABAergic transmission at both pre-and postsynaptic sites in rat central
amygdala neurons. Proceedings of the National Academy of Sciences, 100, 2053-2058.
Rose, A. K., & Duka, T. (2008). Effects of alcohol on inhibitory processes. Behavioural
Pharmacology, 19, 284-291.
Ross, H. E., Cole, C. D., Smith, Y., Neumann, I. D., Landgraf, R., Murphy, A. Z., & Young,
L. J. (2009). Characterization of the oxytocin system regulating affiliative behavior in
female prairie voles. Neuroscience, 162, 892-903.
Rosso, A. M. (2012). Beer and wine in antiquity: beneficial Remedy or punishment imposed
by the Gods? Acta Medico-Historica Adriatica, 10, 237-262.
Roth-Hanania, R., Davidov, M., & Zahn-Waxler, C. (2011). Empathy development from 8 to
16 months: Early signs of concern for others. Infant Behavior and Development, 34, 447-
458.
Sabihi, S., Durosko, N. E., Dong, S. M., & Leuner, B. (2014). Oxytocin in the prelimbic
medial prefrontal cortex reduces anxiety-like behavior in female and male
rats. Psychoneuroendocrinology, 45, 31-42.
Sayette, M. A., Creswell, K. G., Dimoff, J. D., Fairbairn, C. E., Cohn, J. F., Heckman, B. W.,
... & Moreland, R. L. (2012). Alcohol and group formation a multimodal investigation of
the effects of alcohol on emotion and social bonding. Psychological Science. doi:
10.1177/0956797611435134.
Sayette, M. A., Smith, D. W., Breiner, M. J., & Wilson, G. T. (1992). The effect of alcohol
on emotional response to a social stressor. Journal of Studies on Alcohol and Drugs, 53,
541-545.
Schuckit, M. A., & Hesselbrock, V. (1994). Alcohol dependence and anxiety disorders: what
is the relationship? The American Journal of Psychiatry, 151, 1723-1734.
Schulze, L., Lischke, A., Greif, J., Herpertz, S. C., Heinrichs, M., & Domes, G. (2011).
Oxytocin increases recognition of masked emotional faces.
Psychoneuroendocrinology, 36, 1378-1382.
Seltzer, L. J., Ziegler, T., Connolly, M. J., Prososki, A. R., & Pollak, S. D. (2014).
Stressinduced elevation of oxytocin in maltreated children: Evolution,
neurodevelopment, and social behavior. Child Development, 85, 501-512.
Shahrestani, S., Kemp, A. H., & Guastella, A. J. (2013). The impact of a single
administration of intranasal oxytocin on the recognition of basic emotions in humans: a
meta-analysis. Neuropsychopharmacology, 38, 1929-1936.
Shalvi, S., & De Dreu, C. K. (2014). Oxytocin promotes group-serving
dishonesty. Proceedings of the National Academy of Sciences, 111, 5503-5507.
Shamay-Tsoory, S. G. (2011). The neural bases for empathy. Neuroscientist 17, 1824.
Shamay-Tsoory, S. G., Abu-Akel, A., Palgi, S., Sulieman, R., Fischer-Shofty, M., Levkovitz,
Y., & Decety, J. (2013). Giving peace a chance: oxytocin increases empathy to pain in
the context of the IsraeliPalestinian conflict. Psychoneuroendocrinology, 38, 3139-
3144.
Shamay-Tsoory, S. G., Aharon-Peretz, J., & Perry, D. (2009). Two systems for empathy: a
double dissociation between emotional and cognitive empathy in inferior frontal gyrus
versus ventromedial prefrontal lesions. Brain, 132, 617-627.
Shamay-Tsoory, S. G., Fischer, M., Dvash, J., Harari, H., Perach-Bloom, N., & Levkovitz, Y.
(2009). Intranasal administration of oxytocin increases envy and schadenfreude
(gloating). Biological Psychiatry, 66, 864-870.
Sheng, F., Liu, Y., Zhou, B., Zhou, W., & Han, S. (2013). Oxytocin modulates the racial bias
in neural responses to others’ suffering. Biological Psychology, 92, 380-386.
Striepens, N., Kendrick, K. M., Hanking, V., Landgraf, R., Wüllner, U., Maier, W., &
Hurlemann, R. (2013). Elevated cerebrospinal fluid and blood concentrations of oxytocin
following its intranasal administration in humans. Scientific Reports, 3.
doi:10.1038/srep03440
Sripada, C. S., Angstadt, M., McNamara, P., King, A. C., & Phan, K. L. (2011). Effects of
alcohol on brain responses to social signals of threat in humans. Neuroimage, 55, 371-
380.
Stallen, M., De Dreu, C. K., Shalvi, S., Smidts, A., & Sanfey, A. G. (2012). The herding
hormone oxytocin stimulates in-group conformity. Psychological Science, 23, 1288-
1292.
Steele, C. M., Critchlow, B., & Liu, T. J. (1985). Alcohol and social behavior: II. The helpful
drunkard. Journal of Personality and Social Psychology, 48, 35-46.
Stevens, S., Gerlach, A. L., & Rist, F. (2008). Effects of alcohol on ratings of emotional
facial expressions in social phobics. Journal of Anxiety Disorders, 22, 940-948.
Stewart, S. H., Finn, P. R., & Pihl, R. O. (1995). A dose-response study of the effects of
alcohol on the perceptions of pain and discomfort due to electric shock in men at high
familial-genetic risk for alcoholism. Psychopharmacology, 119, 261-267.
Tang, Y., Chen, Z., Tao, H., Li, C., Zhang, X., Tang, A., & Liu, Y. (2014). Oxytocin
activation of neurons in ventral tegmental area and interfascicular nucleus of mouse
midbrain. Neuropharmacology, 77, 277-284.
Theodoridou, A., Rowe, A. C., Penton-Voak, I. S., & Rogers, P. J. (2009). Oxytocin and
social perception: oxytocin increases perceived facial trustworthiness and
attractiveness. Hormones and Behavior, 56, 128-132.
Uvnäs-Moberg, K. (1998). Oxytocin may mediate the benefits of positive social interaction
and emotions. Psychoneuroendocrinology, 23, 819-835.
Vanderbilt, K. E., Liu, D., & Heyman, G. D. (2011). The development of distrust. Child
Development, 82, 1372-1380.
Veroude, K., Jolles, J., Croiset, G., & Krabbendam, L. (2013). Changes in neural mechanisms
of cognitive control during the transition from late adolescence to young
adulthood. Developmental Cognitive Neuroscience, 5, 63-70.
Vijayakumar, N., Whittle, S., Yücel, M., Dennison, M., Simmons, J., & Allen, N. B. (2013).
Prefrontal Structural Correlates of Cognitive Control during Adolescent Development: A
4-Year Longitudinal Study. Journal of Cognitive Neuroscience, 26, 1118-1130
Viviani, D., Terrettaz, T., Magara, F., & Stoop, R. (2010). Oxytocin enhances the inhibitory
effects of diazepam in the rat central medial amygdala. Neuropharmacology, 58, 62-68.
Waldherr, M., & Neumann, I. D. (2007). Centrally released oxytocin mediates mating-
induced anxiolysis in male rats. Proceedings of the National Academy of Sciences, 104,
16681-16684.
Warneken, F., & Tomasello, M. (2008). Extrinsic rewards undermine altruistic tendencies in
20-month-olds. Developmental Psychology, 44, 1785.
Warneken, F., & Tomasello, M. (2009). Varieties of altruism in children and
chimpanzees. Trends in Cognitive Sciences, 13, 397-402.
Windle, R. J., Shanks, N., Lightman, S. L., & Ingram, C. D. (1997). Central Oxytocin
Administration Reduces Stress-Induced Corticosterone Release and Anxiety Behavior in
Rats 1. Endocrinology, 138, 2829-2834.
Xiao, C., & Ye, J. H. (2008). Ethanol dually modulates GABAergic synaptic transmission
onto dopaminergic neurons in ventral tegmental area: role of μ-opioid
receptors. Neuroscience, 153, 240-248.
Young, L. J., & Wang, Z. (2004). The neurobiology of pair bonding. Nature Neuroscience, 7,
1048-1054.
Zak, P. J., Stanton, A. A., & Ahmadi, S. (2007). Oxytocin increases generosity in
humans. PLoS One, 2, e1128.
Figure 1
Cartoon to illustrate the amygdala circuitry underlying OT and GABA
mediated neurotransmission.
Oxytocin acts at presynaptic oxytocin receptors to induce a massive release of
GABA from neurons in the central amygdala nuclei, while both
benzodiazepines and alcohol act synergistically with GABA post-synaptically
(Viviani et al., 2010). Both mechanisms will result in opening of the GABA-A
receptor associated chloride ion channel and so lead to inhibition of the
postsynaptic neuron. Equivalent circuits can be found in the prefrontal cortex.
... However, many studies now indicate that OT is a fundamental molecule for social behavior [18][19][20][21][22][23]. In humans, it has been reported that OT administration promotes social cognition and prosociality in interpersonal relationships among typically developing individuals [24][25][26][27][28]. Consequently, the results of these studies led to the notion that OT may be beneficial for patients with the core symptoms of ASD [29][30][31][32][33][34]. ...
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Background Autism spectrum disorder (ASD) is characterized by the core symptoms of impaired social interactions. Increasing evidence suggests that ASD has a strong genetic link with mutations in chromodomain helicase DNA binding protein 8 (CHD8), a gene encoding a chromatin remodeler. It has previously been shown that Chd8 haplodeficient male mice manifest ASD-like behavioral characteristics such as anxiety and altered social behavior. Along with that, oxytocin (OT) is one of the main neuropeptides involved in social behavior. Administration of OT has shown improvement of social behavior in genetic animal models of ASD. The present study was undertaken to further explore behavioral abnormalities of Chd8 haplodeficient mice of both sexes, their link with OT, and possible effects of OT administration. First, we performed a battery of behavioral tests on wild-type and Chd8+/∆SL female and male mice. Next, we measured plasma OT levels and finally studied the effects of intraperitoneal OT injection on observed behavioral deficits. Results We showed general anxiety phenotype in Chd8+/∆SL mice regardless of sex, the depressive phenotype in Chd8+/∆SL female mice only and bidirectional social deficit in female and male mice. We observed decreased level of OT in Chd+/∆SL mice, possibly driven by males. Mice injected by OT demonstrated recovery of social behavior, while reduced anxiety was observed only in male mice. Conclusions Here, we demonstrated that abnormal social behaviors were observed in both male and female Chd8+/∆SL mice. The ability of peripheral OT administration to affect such behaviors along with altered plasma OT levels indicated a possible link between Chd8 + /∆SL and OT in the pathogenesis of ASD as well as the possible usefulness of OT as a therapeutic tool for ASD patients with CHD8 mutations.
... In most previous studies on craving in substance use disorders (alcohol as well as illicit drugs), doses have been varied from 24 to 40 IU (Pedersen et al. 2013;Lee et al. 2014;Mitchell et al. 2015;Miller et al. 2016;Melby et al. 2019). Our patients were given the opportunity to use nasal spray as needed, 8 IU per dose, until a maximum daily dose of 24 IU. ...
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Aims The aim of this study was to assess the efficacy of self-administered intranasal oxytocin on alcohol dependence after detoxification. Methods In a double-blind, randomized, placebo-controlled trial, 38 patients fulfilling the criteria for ICD-10 diagnosis of alcohol dependence received either 8 IU oxytocin or placebo at their own discretion up to thrice daily for 4 weeks, after completing detoxification. Primary outcome was alcohol intake specified as the amount of alcohol consumed, the number of days to relapse into alcohol use and the proportion of subjects relapsing. Secondary outcomes were self-reported symptoms of craving, sleep and mental distress. Results There were no significant differences between the oxytocin group and the placebo group in daily alcohol intake in total (mean 1.3 ± 2.9 vs. 2.0 ± 5.0 units; P = 0.63) or on drinking days (mean 8.4 ± 2.7 vs. 7.7 ± 6.0 units; P = 0.76), in the number of days until relapse (P = 0.91) or in the proportion of subjects relapsing (37.5 vs. 41.2%; P = 0.84). Neither were there any statistically significant differences in any other outcomes, except a larger decrease in self-reported nervousness in the oxytocin group (P = 0.022). Conclusion The results were inconclusive as to whether intranasal oxytocin reduced the time to relapse, degree of craving or total amount of alcohol consumed after detoxification. However, the oxytocin group had a larger decrease in self-reported nervousness.
... In healthy people, a single application of oxytocin not only improves the recognition of happy faces but also that of fearful and angry faces (Shahrestani et al., 2013). Moreover, in addition to increasing pro-social behaviour, oxytocin can also increase aggressive behaviour (Mitchell et al., 2015). In the area of antidepressants, there was initially historical hope of a 'happiness pill', but in general, the mood-enhancing effects of chronic antidepressant intake in healthy people are at best weak, although there are relatively few studies investigating this. ...
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The use of cognitive-enhancing drugs by healthy individuals has been a feature for much of recorded history. Cocaine and amphetamine are modern cases of drugs initially enthusiastically acclaimed for enhancing cognition and mood. Today, an increasing number of healthy people are reported to use cognitive-enhancing drugs, as well as other interventions, such as non-invasive brain stimulation, to maintain or improve work performance. Cognitive-enhancing drugs, such as methylphenidate and modafinil, which were developed as treatments, are increasingly being used by healthy people. Modafinil not only affects ‘cold’ cognition, but also improves ‘hot’ cognition, such as emotion recognition and task-related motivation. The lifestyle use of ‘smart drugs’ raises both safety concerns as well as ethical issues, including coercion and increasing disparity in society. As a society, we need to consider which forms of cognitive enhancement (e.g. pharmacological, exercise, lifelong learning) are acceptable and for which groups under what conditions and by what methods we would wish to improve and flourish.
... Generally, OXT increases the GABA interneuron functioning, strengthening the signal-to-noise ratio in the principal cell circuits, although it has been demonstrated only in animals so far (Baribeau and Anagnostou, 2015). The stimulating effect of OXT on GABA system has been suggested also in the dlPFC, where increased GABAergic transmission determines the removal of inhibitory brakes which normally act to suppress the expression of response tendencies that are characteristic of earlier developmental stages, as observed in humans (Mitchell et al., 2015). Moreover, OXT activity within raphe nuclei facilitates 5-HT release in this area, thus promoting an anxiolytic effect and decreasing aggressive behaviours. ...
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The human social brain is complex. Current knowledge fails to define the neurobiological processes underlying social behaviour involving the (patho-) physiological mechanisms that link system-level phenomena to the multiple hierarchies of brain function. Unfortunately, such a high complexity may also be associated with a high susceptibility to several pathogenic interventions. Consistently, social deficits sometimes represent the first signs of a number of neuropsychiatric disorders including schizophrenia (SCZ), Alzheimer's disease (AD) and major depressive disorder (MDD), which lead to a progressive social dysfunction. In the present review we summarize present knowledge linking neurobiological substrates sustaining social functioning, social dysfunction and social withdrawal in major psychiatric disorders. Interestingly, AD, SCZ, and MDD affect the social brain in similar ways. Thus, social dysfunction and its most evident clinical expression (i.e., social withdrawal) may represent an innovative transdiagnostic domain, with the potential of being an independent entity in terms of biological roots, with the perspective of targeted interventions.
... [1][2][3][4] Other studies have explored the effects of intranasal oxytocin on symptoms and social dysfunction in patients with psychological or physical disorders. [5][6][7][8][9][10][11][12][13] Evidence from recent studies suggests that the effect of intranasal oxytocin on social cognition varies depending on the social context and individual characteristics. [14][15][16] For example, intranasal oxytocin effects may differ based on gender, [17][18][19] attachment style, 14,20 Print ISSN 1738-3684 / On-line ISSN 1976-3026 OPEN ACCESS and in-group/out-group. ...
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Objective: Research has shown that intranasal oxytocin affects social cognition and behavior; however, its effects vary based on social context, individual characteristics and dose. The present study aimed to determine effective dose of oxytocin spray on emotion recognition in healthy Korean males. Methods: The study followed a randomized, double-blind, placebo-controlled design. Thirty-seven Korean males underwent two experimental sessions, with one week in between. They received either 32 (n=19) or 40 (n=18) international units (IU) of oxytocin and placebo, and then completed a face emotion recognition task. The effect of oxytocin on emotion recognition was examined using repeated measures analysis of variance (ANOVA) for each dose condition. Results: The higher dose (40 IU) was found to improve recognition of happy faces, while the lower dose (32 IU) had no effect. There were no statistical differences in age, education, attachment style or empathic ability between the two dose groups. Conclusion: The results suggest that oxytocin increases the ability of Korean males to recognize positive emotion, and this effect is dose-dependent. Additional studies evaluating the effect of higher doses of oxytocin on social cognition will help to determine the optimal dose for Korean populations.
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Oxytocin (OT) has gained considerable interest in recent years as a potential treatment for alcoholism and other substance use disorders. Evidence continues to mount that OT administered either centrally, peripherally or intranasally can decrease ethanol intake in both humans and animal models. The potential mechanisms for the ability of OT to decrease ethanol reward, and importantly, cue- and stress-induced ethanol relapse, are explored by reviewing the specific neuronal circuits involved in mediating these actions and their sensitivity to OT. In addition to dopamine neurons that project from ventral tegmental area (VTA) to nucleus accumbens (NAc) to signal positively reinforcing events, OT receptors (OxTR) are also expressed by dopamine neurons that project from VTA to brain regions that can convey aversive properties of a stimulus. Moreover, OxTR are expressed by non-dopaminergic neurons in the VTA, such as GABA and glutamate neurons, which can both modulate the activity of dopamine VTA neurons locally (in opposite directions) or can project to other brain regions, including the NAc, where it can alter either positive reinforcement or aversion caused by ethanol. The ability of OT to regulate limbic circuitry and the hypothalamic-pituitary-adrenal axis is discussed as a potential mechanism for the ability of OT to inhibit ethanol-induced negative reinforcement. Together, understanding the diversity and complexity of OT regulation of ethanol reward may contribute to more effective use of OT as pharmacotherapy for alcohol use disorder. This article is part of the special issue on Neuropeptides.
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The neuropeptide oxytocin (OT) may be beneficial to augmenting behavioral therapies for couples given its ability to alleviate stress reactivity and increase pro-social behavior. However, there is growing evidence demonstrating inconsistent effects of OT on social behavior. Infidelity may represent a relational vulnerability that modulates the OT response. The present study hypothesized that actor and partner emotional and physical infidelity would be associated with less adaptive conflict behaviors, and moderate the OT response, such that participants randomized to a OT condition, compared to placebo, who report more infidelity would show less adaptive conflict behaviors. Participants were 30 couples (N = 60) wherein one or both partners engaged in recent hazardous drinking or illicit drug use. Partners completed a 10-min dyadic conflict task in the laboratory, self-administered a single intranasal dose of OT (40 IU) or placebo, and then completed the same 10-min dyadic conflict task following a 45-min wait period. Couple conflict behaviors were observed during the conflict tasks and assessed using a validated coding system. Actor partner interdependence models detected significant interactions between drug condition and physical infidelity, such that among individuals in the OT group, verses individuals in the placebo group, (a) who reported greater physical infidelity had greater distress maintaining attributions and (b) whose partners reported greater physical infidelity had fewer relationship enhancing attributions. Results are consistent with the social salience hypothesis of OT and suggest that physical infidelity appears to serve as a contextual vulnerability that may decreases positive and increase negative behaviors during conflict. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
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El objetivo de este artículo es mostrar una nueva herramienta capaz de garantizar una formación personalizada, predictiva, preventiva y precisa basada en el análisis del persotipo del ADN emocional (ADNe), lo que nos permite identificar la adecuación que posee y el método de corrección requerido en cada individuo para asimilar conocimientos teóricos y prácticos. Su utilidad en el es enorme al permitir una completa gestión del talento individual y colectivo con respecto a los logros académicos y profesionales a alcanzar.
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Combining pharmacological interventions with evidence-based behavioral interventions may help optimize treatment outcomes for alcohol use disorder (AUD). While several effective behavioral interventions for AUD have been developed, the vast majority target individual patients, despite evidence that behavioral interventions for couples have the ability to outperform individual treatments for AUD. Alcohol Behavioral Couples Therapy (ABCT) is an evidence-based behavioral intervention for couples that has been shown to significantly reduce AUD severity as well as improve relationship functioning. Accumulating evidence suggests that the neuropeptide oxytocin has the ability to reduce alcohol craving and consumption, symptoms of tolerance and withdrawal, and ameliorate neurobiological deficits associated with AUD. Furthermore, oxytocin has demonstrated the ability to increase prosocial behavior and cognition, and restore sensitivity to natural rewards such as interpersonal relationships. No study to date has examined the ability of oxytocin to enhance ABCT. Thus, the primary objective of this Phase II study is to examine the effects of oxytocin versus placebo in combination with ABCT in reducing AUD severity and improving relationship functioning. We also will utilize neuroimaging techniques before and after treatment to investigate the underlying pathophysiology of AUD among couples and identify prognostic indicators of treatment outcome. The findings from this study might provide critical new information to help inform clinical practice and accelerate research on the pharmacological treatment of AUD.
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Introduction Preclinical and clinical evidence suggest that the neuropeptide oxytocin may be of value in treating alcohol use disorder, either by reducing the rewarding effects of alcohol or reducing negative affect induced by alcohol withdrawal. However, the effect of a single dose of oxytocin on subjective and psychomotor responses to alcohol in social drinkers is not known. Methods The present study examined the effect of intranasal oxytocin on subjective, behavioral, and physiological responses to a moderate dose of alcohol (0.8 g/kg) in young adult social drinkers. Participants (N=35) completed two study sessions at which they consumed beverages containing alcohol (ALC; N=20) or placebo (NoALC; N=15) in combination with intranasal oxytocin (40 IU with a 20 IU booster) or placebo. They received oxytocin at one session and placebo at the other session (order counterbalanced) 20 min before consuming beverages. Subjective mood and drug effects ratings, heart rate and blood pressure, and four behavioral tasks (flanker task, digit span, go/no‐go, and pursuit rotor) were the primary outcome measures. Results ALC produced its expected subjective and behavioral effects; including feeling intoxicated and impaired performance on the digit span and go/no‐go tasks. Oxytocin alone had no significant subjective or physiological effects, and it did not affect responses to alcohol on any measure. Conclusion We can conclude that, under these conditions, a single dose of intranasal oxytocin does not alter the effects of acute alcohol in healthy young adult social drinkers. Further research is needed to determine whether oxytocin alters responses to alcohol under different conditions, and to determine its potential as an aid in treatment for substance use disorders. This article is protected by copyright. All rights reserved.
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Studies have consistently shown that both consumption of acute amounts of alcohol an elevated antisocial psychopathic traits are associated with an impaired ability for prepoten response inhibition. This may manifest as a reduced ability to inhibit prepotent race biase responses. Here, we tested the effects of acute alcohol consumption, and elevated anti social psychopathic traits, on judgments of the attractiveness and health of ethnic ingrou and outgroup faces. In the first study, we show that following acute alcohol consumption at a dose that is sufficient to result in impaired performance on tests of executive function Caucasian participants judged White faces to be more attractive and healthier compared t when sober. However, this effect did not extend to Black faces. A similar effect was foun in a second study involving sober Caucasian participants where secondary psychopathi traits were related to an intergroup bias in the ratings of attractiveness for White versu Black faces. These results are discussed in terms of a model which postulates that poo prefrontal functioning leads to increases in ingroup liking as a result of impaired abilitie for prepotent response inhibition. d t d-p , , o d c s r s
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Oxytocin (OT) knock-out mice fail to recognize familiar conspecifics after repeated social exposures, despite normal olfactory and spatial learning abilities. OT treatment fully restores social recognition. Here we demonstrate that OT acts in the medial amygdala during the initial exposure to facilitate social recognition. OT given before, but not after, the initial encounter restores social recognition in OT knock-out mice. Using c-Fos immunoreactivity (Fos-IR) as a marker of neuronal activation in this initial encounter, we found similar neuronal activation in the wild-type (WT) and OT knock-out mouse in olfactory bulbs, piriform cortex, cortical amygdala, and the lateral septum. Wild-type, but not OT knock-out mice exhibited an induction of Fos-IR in the medial amygdala. Projections sites of the medial amygdala also failed to show a Fos-IR induction in the OT knock-out mice. OT knock-out, but not WT, mice showed dramatic increases in Fos-IR in the somatosensory cortex and the hippocampus, suggesting alternative processing of social cues in these animals. With site-specific injections of OT and an OT antagonist, we demonstrate that OT receptor activation in the medial amygdala is both necessary and sufficient for social recognition in the mouse.
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Does oxytocin influence intimate partner violence (IPV)? Clues from prior research suggest that oxytocin increases prosocial behavior, but this effect is reversed among people with aggressive tendencies or in situations involving defensive aggression. Animal research also indicates that oxytocin plays a central role in defensive maternal aggression (i.e., protecting pups from intruders). Among highly aggressive people, a boost of oxytocin may cause them to use aggression toward close others as a means of maintaining their relationship. Adopting an interactionist approach, we predicted that oxytocin would increase IPV inclinations, but this effect would be limited to people high in trait physical aggression. In a double-blind, placebo-controlled, between-subject experiment, participants varying in trait physical aggression received either 24 international unit of oxytocin or a placebo. Following two provocation tasks, participants rated the probability that they would engage in various aggressive behaviors (e.g., slapping, throwing an object that could hurt) toward a romantic partner. Oxytocin increased IPV inclinations, but this effect was limited to participants prone to physical aggression. These data offer the first evidence that IPV inclinations have a biological basis in a combination of oxytocin and trait physical aggressiveness.
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Endocrine responses to noise stress and anxiety-related behaviors were measured in groups of ovariectomized, estradiol-treated female rats given central infusions of oxytocin. Control animals receiving isotonic saline showed a large increase in plasma corticosterone concentrations in response to 10 min of white noise. This response to noise stress was significantly and dose dependently decreased by oxytocin administered intracerebroventricularly at 10 or 100 ng/h for 5 days. Oxytocin also significantly decreased rearing behavior during this stress. When a second noise stress was given 3 days after cessation of oxytocin infusion, corticosterone responses did not differ between the control and previously oxytocin-infused animals. Administration of vasopressin had no significant effect on either the corticosterone or behavioral responses to noise stress. Anxiety-related behaviors were measured on the elevated plus-maze. No significant differences were seen in maze exploration between saline- and oxytocin-treated animals when housed and tested in the same environment. However, when animals were mildly stressed by testing in an unfamiliar environment, oxytocin-treated animals showed a higher proportion of open arm entries and spent significantly more time in the open arms of the maze. Thus, oxytocin exerts a central anxiolytic-like effect on both endocrine and behavioral systems and could play a role in moderating behavioral and physiological responses to stress.
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Accumulating evidence demonstrates the important role of oxytocin (OT) in the modulation of social cognition and behavior. This has led many to suggest that the intranasal administration of OT may benefit psychiatric disorders characterized by social dysfunction, such as autism spectrum disorders and schizophrenia. Here, we review nasal anatomy and OT pathways to central and peripheral destinations, along with the impact of OT delivery to these destinations on social behavior and cognition. The primary goal of this review is to describe how these identified pathways may contribute to mechanisms of OT action on social cognition and behavior (that is, modulation of social information processing, anxiolytic effects, increases in approach-behaviors). We propose a two-level model involving three pathways to account for responses observed in both social cognition and behavior after intranasal OT administration and suggest avenues for future research to advance this research field.