Mary C Olmstead

Queens University of Charlotte, Charlotte, North Carolina, United States

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Publications (73)234.15 Total impact

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    ABSTRACT: Opioid dependence is accompanied by neuroplastic changes in reward circuitry leading to a negative affective state contributing to addictive behaviors and risk of relapse. The current study presents a neuroimmune mechanism through which chronic opioids disrupt ventral tegmental area (VTA) dopaminergic circuitry that contributes to impaired reward behavior. Opioid dependence was produced in rodents by treating with escalating doses of morphine. Microglial activation was observed in the VTA following spontaneous withdrawal from chronic morphine treatment. Opioid-induced microglial activation resulted in an increase in brain derived neurotrophic factor (BDNF) expression and a reduction in the expression and function of the K(+)Cl(-) co-transporter KCC2 within VTA GABAergic neurons. Inhibition of microglial activation or interfering with BDNF signaling prevented the loss of Cl(-) extrusion capacity and restored the rewarding effects of cocaine in opioid-dependent animals. Consistent with a microglial-derived BDNF-induced disruption of reward, intra-VTA injection of BDNF or a KCC2 inhibitor resulted in a loss of cocaine-induced place preference in opioid-naïve animals. The loss of the extracellular Cl(-) gradient undermines GABAA-mediated inhibition, and represents a mechanism by which chronic opioid treatments can result in blunted reward circuitry. This study directly implicates microglial-derived BDNF as a negative regulator of reward in opioid-dependent states, identifying new therapeutic targets for opiate addictive behaviors.Neuropsychopharmacology accepted article preview online, 23 July 2015. doi:10.1038/npp.2015.221.
    Full-text · Article · Jul 2015 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
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    ABSTRACT: Chronic pain attenuates midbrain dopamine (DA) transmission, as evidenced by a decrease in opioid-evoked DA release in the ventral striatum, suggesting that the occurrence of chronic pain impairs reward-related behaviors. However, mechanisms by which pain modifies DA transmission remain elusive. Using in vivo microdialysis and microinjection of drugs into the mesolimbic DA system, we demonstrate in mice and rats that microglial activation in the VTA compromises not only opioid-evoked release of DA, but also other DA-stimulating drugs, such as cocaine. Our data show that loss of stimulated extracellular DA is due to impaired chloride homeostasis in midbrain GABAergic interneurons. Treatment with minocycline or interfering with BDNF signaling restored chloride transport within these neurons and recovered DA-dependent reward behavior. Our findings demonstrate that a peripheral nerve injury causes activated microglia within reward circuitry that result in disruption of dopaminergic signaling and reward behavior. These results have broad implications that are not restricted to the problem of pain, but are also relevant to affective disorders associated with disruption of reward circuitry. Because chronic pain causes glial activation in areas of the CNS important for mood and affect, our findings may translate to other disorders, including anxiety and depression, that demonstrate high comorbidity with chronic pain. Copyright © 2015 Taylor et al.
    Full-text · Article · Jun 2015 · The Journal of Neuroscience : The Official Journal of the Society for Neuroscience
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    S A Magrys · M C Olmstead
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    ABSTRACT: The primary aim of this study was to assess whether an acute stressor directly increases alcohol intake among undergraduates. A secondary aim was to examine whether individual differences in state anxiety predict alcohol intake. Following random assignment, undergraduate students (n = 75; 47% males; mean age = 20.1 ± 2.8) completed the Trier Social Stress Test or no-stress protocol, and then engaged in a 30-min free-drinking session (alcohol, placebo, or non-alcoholic beverage). The State-Trait Anxiety Inventory was completed upon arrival, post-stressor, and after drinking. Planned comparisons demonstrated that psychosocial stress increased voluntary intake of alcohol, but not placebo or non-alcoholic beverages. In linear regression analyses, individual differences in anxiety did not predict voluntary alcohol consumption. A proximal relationship exists between acute stress and single-session alcohol intake in undergraduates, which may explain the relationship between life stressors and increased drinking in this group. These findings demonstrate that stress management is an important target for reducing heavy episodic drinking on university campuses. © The Author 2015. Medical Council on Alcohol and Oxford University Press. All rights reserved.
    Preview · Article · Jan 2015 · Alcohol and alcoholism (Oxford, Oxfordshire). Supplement
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    E W Ong · L Xue · M C Olmstead · C M Cahill
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    ABSTRACT: Background and purposeThe delta opioid receptor (DOPr) undergoes internalisation both constitutively and in response to agonists. Previous work has shown DOPr to traffic from intracellular compartments to neuronal cell membranes following prolonged morphine treatment. Here, we examined the effects of prolonged morphine treatment on the post-internalisation trafficking of DOPr.Experimental approachUsing primary cultures of dorsal root ganglia (DRG) neurons, we measured the co-localisation of endogenous DOPr with post-endocytic compartments following both prolonged and acute agonist treatments.Key resultsWe first show a departure from the constitutive trafficking pathway following acute DOPr agonist-induced internalisation by Deltorphin II. That is, DOPr undergoes distinct agonist-induced post-endocytic sorting. Second, we demonstrate an augmentation of constitutive DOPr trafficking following prolonged morphine treatment. Third, we show an unmasking of similar DOPr agonist-induced post-endocytic sorting by SNC80 following prolonged morphine treatment. Fourth, we show that the mu opioid receptor (MOPr) agonist DAMGO induces DOPr internalisation and trafficking following prolonged morphine. Finally, we show that all of the alterations to DOPr trafficking induced by both DOPr and MOPr agonists are inhibited or absent when those agonists are co-administered with a DOPr antagonist, SDM-25N.Conclusions and ImplicationsThe results support the hypothesis that prolonged morphine treatment induces the formation of MOPr-DOPr interactions and subsequent augmentation of cell surface available DOPr, at least some of which are in the form of a M/DOPr species. Such a species appears to have pharmacology and trafficking unique from those of its individual constituents.
    Full-text · Article · May 2014 · British Journal of Pharmacology
  • S.A. Magrys · M.C. Olmstead
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    ABSTRACT: Alcohol intoxication affects frontal and temporal brain areas and may functionally impair cognitive processes mediated by these regions. This study examined this hypothesis by testing the effects of alcohol on sustained attention, impulsivity, and verbal memory. Sober and placebo control groups were used to distinguish pharmacological from expectancy effects of alcohol. One hundred nine university students were assigned to an alcohol (low, medium, or high dose), placebo or sober group. Moderate and high doses of alcohol impaired all cognitive measures. A gender effect was revealed in that alcohol impaired sustained attention in males, but not females. Both sustained attention and verbal memory exhibited a U-shaped pattern, in that the medium-dose alcohol group showed the greatest impairment. This study adds to knowledge about the effects of alcohol intoxication on frontally- and temporally-mediated cognitive function. These findings have specific relevance for heavy-drinking undergraduate populations, particularly in light of the fact that repeated alcohol administration produces persistent changes in brain neurocircuitry.
    No preview · Article · Jan 2014 · Brain and Cognition
  • S.A. Magrys · M.C. Olmstead
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    ABSTRACT: Alcohol intoxication affects frontal and temporal brain areas and may functionally impair cognitive processes mediated by these regions. This study examined this hypothesis by testing the effects of alcohol on sustained attention, impulsivity, and verbal memory. Sober and placebo control groups were used to distinguish pharmacological from expectancy effects of alcohol. One hundred nine university students were assigned to an alcohol (low, medium, or high dose), placebo or sober group. Moderate and high doses of alcohol impaired all cognitive measures. A gender effect was revealed in that alcohol impaired sustained attention in males, but not females. Both sustained attention and verbal memory exhibited a U-shaped pattern, in that the medium-dose alcohol group showed the greatest impairment. This study adds to knowledge about the effects of alcohol intoxication on frontally- and temporally-mediated cognitive function. These findings have specific relevance for heavy-drinking undergraduate populations, particularly in light of the fact that repeated alcohol administration produces persistent changes in brain neurocircuitry.
    No preview · Article · Jan 2014 · Brain and Cognition
  • Megan K. Mahoney · Kyle Cogger · Tanya Tran · Mary C. Olmstead

    No preview · Article · Oct 2013 · Behavioural Pharmacology
  • Megan K Mahoney · Mason M Silveira · Mary C Olmstead
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    ABSTRACT: Impulsive action is mediated through several neurochemical systems, although it is not clear which role each of these plays in the inability to withhold inappropriate responses. Manipulations of the opioid system alter impulsive action in rodents, although the effects are not consistent across tasks. Previously, we speculated that these discrepancies reflect differences in the cognitive mechanisms that control responding in each task. We investigated whether the effect of morphine, a mu opioid receptor (MOR) agonist, on impulsive action depends on the ability of the subjects to time the interval during which they must inhibit a response. Male Long-Evans rats were trained in a response inhibition (RI) task to withhold responding for sucrose during a 4- or 60-s delay; impulsive action was assessed as increased responding during the delay. The rats were tested following an injection of morphine (0, 1, 3, 6 mg/kg). In a subsequent experiment, the effects of morphine (6 mg/kg) plus the MOR antagonist naloxone (0, 0.3, 1, 3 mg/kg) were investigated. Morphine increased impulsive action, but had different effects in the two conditions: the drug increased the proportion of premature responses as the 4-s interval progressed and produced a general increase in responding across the 60-s interval. Naloxone blocked all morphine-induced effects. The finding that morphine increases impulsive action in a fixed-delay RI task contrasts with our previous evidence which shows no effect in the same task with a variable delay. Thus, MORs disrupt impulsive action only when rats can predict the delay to respond.
    No preview · Article · Jul 2013 · Psychopharmacology
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    ABSTRACT: In addition to sensory disturbances, neuropathic pain is associated with an ongoing and persistent negative affective state. This condition may be reflected as altered sensitivity to rewarding stimuli. We examined this hypothesis by testing whether the rewarding properties of morphine are altered in a rat model of neuropathic pain. Neuropathic pain was induced by chronic constriction of the common sciatic nerve. Drug reward was assessed using an unbiased, three-compartment conditioned place preference (CPP) paradigm. The rats underwent two habituation sessions beginning 6 days after surgery. Over the next 8 days, they were injected with drug or vehicle and were confined to one CPP compartment for 30 min. On the following test day, the rats had access to all three compartments for 30 min. Consistent with the literature, systemic administration of morphine dose-dependently increased the CPP in pain-naive animals. In rats with neuropathic pain, however, the dose-dependent effects of morphine were in a bell-shaped curve, with a low dose of morphine (2 mg/kg) producing a greater CPP than a higher dose of morphine (8 mg/kg). In a separate group of animals, acute administration of morphine reversed mechanical allodynia in animals with neuropathic pain at the same doses that produced a CPP. The increased potency of systemic morphine to produce a CPP in animals with neuropathic pain suggests that the motivation for opioid-induced reward is different in the two states.
    Full-text · Article · Apr 2013 · Behavioural pharmacology
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    Megan K Mahoney · Mary C Olmstead
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    ABSTRACT: Most adults in Western society consume alcohol on a regular basis with few or no negative consequences. However, for certain individuals, alcohol use escalates, leading to uncontrolled drinking bouts, craving, and repeated episodes of relapse. The transition from regulated to uncontrolled and compulsive drinking is a defining feature (i.e. an endophenotype) of alcohol addiction. This behavioral progression can be modeled in rodent paradigms that parallel the diagnostic criteria for addiction in humans. Using these criteria as a framework, this review outlines the neurobiological factors associated with increased vulnerability to excessive, compulsive, and dysregulated alcohol intake in rodents. We conclude by noting gaps in the literature and outline important directions for future research.
    Full-text · Article · Mar 2013 · Current opinion in neurobiology
  • S A Magrys · M C Olmstead · K E Wynne-Edwards · I M Balodis
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    ABSTRACT: Ambiguous biochemical and subjective responses to alcohol may relate to preexisting individual differences in alcohol expectations, experience, or impulsivity. This study examined cortisol and alpha-amylase responses to alcohol and their association with trait impulsivity, alcohol expectancy, and subjective reports of alcohol's effects. Eighty-seven males assigned to an alcohol, sober, or placebo group provided biochemical and self-report measures. Both cortisol and alpha-amylase increased following alcohol administration. Impulsivity correlated with cortisol changes, and the greatest rise in cortisol correlated with high stimulating effects in the alcohol group. These findings emphasize the importance of individual differences in alcohol responses and support a relationship between hormonal responses and alcohol use.
    No preview · Article · Dec 2012 · Psychophysiology
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    Scott J Hayton · Amanda C Maracle · Mary C Olmstead
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    ABSTRACT: Impulsive action, the failure to withhold an inappropriate response, is treated clinically with dopamine agonists such as amphetamine. Despite the therapeutic efficacy, these drugs have inconsistent effects on impulsive action in rodents, causing improvements or disruptions in different tasks. Thus, we hypothesized that amphetamine is producing an effect by altering distinct cognitive processes in each task. To test this idea, we used the response inhibition (RI) task and trained rats to withhold responding for sucrose until a signal is presented. We then varied the duration that subjects were required to inhibit responding (short=4 s; long=60 s; or variable=1-60 s) and examined whether this influenced the pattern of premature responses. We also tested the effects of amphetamine (0.0, 0.125, 0.25, 0.5, and 1.0 mg/kg) on each task variant. The probability of premature responding varied across the premature interval with a unique pattern of time-dependent errors emerging in each condition. Amphetamine also had distinct effects on each version: the drug promoted premature responding when subjects expected a consistent delay, regardless of its duration, but reduced premature responding when the delay was unpredictable. We propose that the ability to inhibit a motor response is controlled by a different combination of cognitive processes in the three task conditions. These include timing, conditioned avoidance, and attention, which then interact with amphetamine to increase or decrease impulsive action. The effect of amphetamine on impulsive action, therefore, is not universal, but depends on the subject's experience and expectation of the task demands.
    Preview · Article · Feb 2012 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
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    ABSTRACT: The objective of this study was to test the hypothesis that prenatal exposure to ethanol, through maternal consumption of an aqueous ethanol solution, induces neurobehavioral deficits and increases ethanol preference in offspring. Pregnant Dunkin-Hartley-strain guinea pigs were given 24-h access to an aqueous ethanol solution (5%, v/v) sweetened with sucralose (1 g/l), or water sweetened with sucralose (1 g/l), throughout gestation. Spontaneous locomotor activity was measured in the offspring on postnatal day (PD) 10. The offspring underwent either ethanol preference testing using a two-bottle-choice paradigm beginning on PD 40 or Morris water maze testing using a hidden moving platform design beginning on PD 60. Maternal consumption of a 5% (v/v) ethanol solution (average daily dose of 2.3±0.1 g of ethanol/kg maternal body weight; range: 1.8-2.8 g/kg) decreased offspring birth weight, increased spontaneous locomotor activity, and increased preference for an aqueous ethanol solution. In the Morris water maze test, sucralose-exposed offspring decreased escape latency on the second day of testing, whereas the ethanol-exposed offspring showed no improvement. These data demonstrate that moderate maternal consumption of ethanol produces hyperactivity, enhances ethanol preference, and impairs learning and memory in guinea pig offspring.
    Full-text · Article · Dec 2011 · Behavioural pharmacology
  • Scott J Hayton · Megan K Mahoney · Mary C Olmstead
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    ABSTRACT: Most adults in Western society consume alcohol regularly without negative consequences. For a small subpopulation, however, drinking can quickly progress to excessive and chronic intake. Given the dangers associated with alcohol abuse, it is critical to identify traits that may place an individual at risk for developing these behaviors. To that end, we used a rat model to determine whether anxiety-related behaviors, novelty seeking, or cognitive flexibility predict excessive alcohol drinking under both limited and continuous access conditions. Adult male rats were assessed in a series of behavioral tasks (elevated plus maze [EPM], locomotor activity, and discrimination/reversal learning in a Y-maze) followed by 6 weeks of daily, 1-hour access to alcohol in a free-choice, 2-bottle paradigm (10% alcohol vs. tap water). Next, subjects were given the opportunity to consume alcohol for 72 hours in drinking chambers that permit separate measures of each drinking bout. Half of the animals experienced a 2-week deprivation period between the limited and continuous access sessions. Time spent on the open arms of the EPM, but not novelty seeking or discrimination/reversal learning, predicted alcohol consumption during limited, 1-h/d access sessions to alcohol. Anxiety-related behavior also predicted the escalation of intake when animals were given 72 hours of continuous access to alcohol. Bout size, but not frequency, was responsible for the increased consumption by high-anxiety subjects during this period. Finally, intake during limited access sessions predicted intake during continuous access, but only in subjects with low intake during limited access. These findings confirm that preexisting anxiety-related behavior predicts alcohol intake under several schedules of alcohol access. Moreover, when access is unlimited, the high-anxiety-related group exhibited an increase in bout size, but not frequency, of drinking. In addition, we show that modest intake when alcohol is restricted may or may not progress to excessive intake when the drug is freely available.
    No preview · Article · Oct 2011 · Alcoholism Clinical and Experimental Research
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    Scott J Hayton · Mary C Olmstead · Éric C Dumont
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    ABSTRACT: Impulse control is an executive process that allows animals to inhibit their actions until an appropriate time. Previously, we reported that learning a simple response inhibition task increases AMPA currents at excitatory synapses in the prelimbic region of the medial prefrontal cortex (mPFC). Here, we examined whether modifications to intrinsic excitability occurred alongside the synaptic changes. To that end, we trained rats to obtain a food reward in a response inhibition task by withhold responding on a lever until they were signaled to respond. We then measured excitability, using whole-cell patch clamp recordings in brain slices, by quantifying action potentials generated by the injection of depolarizing current steps. Training in this task depressed the excitability of layer V pyramidal neurons of the prelimbic, but not infralimbic, region of the mPFC relative to behavioral controls. This decrease in maximum spiking frequency was significantly correlated with performance on the final session of the task. This change in intrinsic excitability may represent a homeostatic mechanism counterbalancing increased excitatory synaptic inputs onto those neurons in trained rats. Interestingly, subjects trained with a cue that predicted imminent reward availability had increased excitability in infralimbic, but not the prelimbic, pyramidal neurons. This dissociation suggests that both prelimbic and infralimbic neurons are involved in directing action, but specialized for different types of information, inhibitory or anticipatory, respectively.
    Full-text · Article · Aug 2011 · PLoS ONE
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    ABSTRACT: Ultralow-dose opioid antagonists augment the antinociceptive effect of morphine and block the development of tolerance to repeated morphine injections in rodents, but the effects are not reliably reproduced in humans. One explanation for this discrepancy is that preclinical studies of ultralow-dose antagonism in rodents generally use reflex-withdrawal tests of antinociception, which may be affected by cataleptic effects of morphine. We tested this hypothesis by examining whether ultralow-dose naltrexone alters the cataleptic effect of morphine or the development of tolerance to morphine-induced catalepsy. Rats (N=56) were randomly assigned to saline, morphine (10 mg/kg), cotreatments of morphine plus naltrexone (molar ratios of 1,000,000 : 1; 500,000 : 1; 100,000 : 1), or naltrexone-alone groups. Rats were injected with drug for 7 consecutive days; on each day, catalepsy and antinociception were assessed 30 and 60 min postinjection, using the bar and tail-flick tests, respectively. Ultralow-dose naltrexone (500,000 : 1) extended the antinociceptive effect of morphine within a session and attenuated the development of tolerance to the antinociceptive effect of morphine across sessions. Naltrexone alone had no effect on either test. These data show that the paradoxical effect of ultralow-dose naltrexone on antinociception is not the product of morphine-induced catalepsy, pointing to an important role for agonist-antagonist combinations in the clinical treatment of pain.
    No preview · Article · May 2011 · Behavioural pharmacology
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    ABSTRACT: This experiment used both biological and self-report measures to examine how alcohol modifies stress responses, and to test whether the interaction between these two factors alters risk-taking in healthy young adults. Participants were divided into stress or no-stress conditions and then further divided into one of three beverage groups. The alcohol group consumed a binge-drinking level of alcohol; the placebo group consumed soda, but believed they were consuming alcohol; the sober group was aware that they were not consuming alcohol. Following beverage consumption, the stress group was subjected to the Trier Social Stress Test (TSST) while the no-stress group completed crossword puzzles; all participants subsequently completed a computerized risk-taking task. Exposure to the TSST significantly increased salivary levels of the hormone cortisol and the enzyme alpha-amylase, as well as subjective self-ratings of anxiety and tension. In the stress condition, both placebo and intoxicated groups reported less tension and anxiety, and exhibited a smaller increase in cortisol, following the TSST than did the sober group. Thus, the expectation of receiving alcohol altered subjective and physiological responses to the stressor. Neither alcohol nor stress increased risk taking, however the sober group demonstrated lower risk-taking on the computer task on the second session. These findings clearly demonstrate that the expectation of alcohol (placebo) alters subsequent physiological responses to stress.
    Full-text · Article · Apr 2011 · Hormones and Behavior
  • Stephanie D. Hancock · Mary C. Olmstead
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    ABSTRACT: Eating disorders and drug addiction share many common traits. This includes biological and environmental factors that predispose individuals to develop either disorder, an increased risk for anxiety and depression when the disorders are present, and heightened trait levels of impulsivity and compulsion. Animal models of eating disorders are not as well established as those that model drug addiction, but the research in this area is progressing rapidly. In this chapter, we discuss anorexia nervosa, bulimia nervosa, binge eating disorder, and obesity as these encompass the majority of maladaptive eating behaviors in humans. We begin by outlining the important features that characterize each disorder and that should thereby be present in an animal model. An overview of peptide control of feeding is provided to help the reader evaluate the animal models presented. These are based principally on genetic variation and stressful life events. In general, most animal models based on genetic alterations have limited applicability to humans, at least to date. Those based on stressful life events appear more promising in that they more accurately reproduce alterations in feeding and neuroendocrine function that are characteristic of each disorder. The next obvious step in eating disorder research is to combine the two approaches to determine how genetic alterations and stressful events interact to produce maladaptive eating and physiological changes. Key wordsAnorexia nervosa–Bulimia nervosa–Binge eating disorder–Obesity–Stress–Genetics–Neuroendocrine function–Feeding peptides–Hypothalamus
    No preview · Chapter · Dec 2010
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    ABSTRACT: Response inhibition, a primary symptom of many psychiatric disorders, is mediated through a complex neuropharmacological network that involves dopamine, serotonin, glutamate, noradrenaline, and cannabinoid mechanisms. Recently, we identified an opioidergic contribution to response inhibition by showing that deletion of mu or delta opioid receptors in mice alters motor impulsivity. We investigated this phenomenon further by testing whether pharmacological activation of opioid receptors disrupts the ability to inhibit a motor response. Long-Evans rats were trained to withhold a lever-pressing response for sucrose until a discriminative stimulus (lever light) was presented. The delay to the discriminative stimulus (1 to 60 s) was varied, so animals could not predict, on any given trial, the length of the pre-response phase. Motor impulsivity was assessed as the inability to inhibit lever pressing prior to the discriminative stimulus. Rats were tested following an injection of the mu opioid receptor agonist morphine (0, 0.5, 1, 2, 4, 6, 8, or 10 mg/kg) or the delta receptor agonist SNC80 (0, 2.5, 5, or 10 mg/kg). SNC80 (10 mg/kg) increased premature responses and locomotor activity, but had no effect on the speed of responding or non-reinforced presses. The SNC80-induced decrease in accuracy was blocked by the delta opioid receptor antagonist naltrindole. Morphine had no effect on accuracy but increased locomotor activity (2 mg/kg). These findings point to a role for delta, but not mu, opioid receptors in disinhibition as measured in the response inhibition task. The results appear to contradict those of previous opioid receptor deletion studies; possible sources of these discrepant results are discussed.
    No preview · Article · Dec 2010 · Psychopharmacology
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    Iris M Balodis · Marc N Potenza · Mary C Olmstead
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    ABSTRACT: The consumption of drugs during young adulthood may be particularly detrimental given important neurodevelopmental changes occurring during this period. As impulsivity may lead to substance use and substance use to the commission of seemingly impulsive acts, an improved understanding of the relationship between alcohol use, other substance use and impulsivity in young adults is important. We gathered information on self-reported impulsivity, recreational drug use, and drinking habits of 205 (105 female) undergraduate students. Results showed that 64% of the students reported using marijuana at least once and these individuals were more likely to report binge drinking. Polysubstance use, defined as using marijuana and at least one other illicit substance, was reported by 20% of students. These individuals reported more drinking occasions per month and had higher levels of trait impulsivity. Rates of recreational drug use were similar to those reported in recent national surveys, suggesting an increase in experimentation with specific illicit drugs. Given that a majority of undergraduate drinkers reported marijuana use and its association with binge drinking, future research should clarify the relationship between marijuana use and binge consumption of alcohol and prevention efforts should consider the conjoint targeting of marijuana and binge drinking. The associations between polysubstance use, binge-level alcohol consumption and elevated self-reported impulsivity suggests that perceived trait impulsivity across multiple domains may predispose to excessive use of multiple substances. Longitudinal studies should examine the contribution of impulsivity to the initiation and experimentation with illicit drugs and the influence of specific substances on impulsivity.
    Preview · Article · Oct 2010 · Frontiers in Psychiatry

Publication Stats

3k Citations
234.15 Total Impact Points

Institutions

  • 1999-2014
    • Queens University of Charlotte
      Charlotte, North Carolina, United States
  • 1998-2014
    • Queen's University
      • • Department of Psychology
      • • Centre for Neuroscience Studies
      Kingston, Ontario, Canada
  • 2003
    • University of Toronto
      • Department of Psychology
      Toronto, Ontario, Canada
  • 1998-2000
    • University of Cambridge
      • Department of Psychology
      Cambridge, England, United Kingdom
  • 1993-1996
    • McGill University
      • Department of Psychology
      Montréal, Quebec, Canada