Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology (Neuropsychopharmacology)

Publisher: Nature Publishing Group, Nature Publishing Group

Journal description

Neuropsychopharmacology is an international scientific journal and the official publication of the American College of Neuropsychopharmacology. The journal focuses on clinical and basic science contributions that advance our understanding of the brain and behavior.

Current impact factor: 7.05

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 7.048
2013 Impact Factor 7.833
2012 Impact Factor 8.678
2011 Impact Factor 7.991
2010 Impact Factor 6.685
2009 Impact Factor 6.993
2008 Impact Factor 6.835
2007 Impact Factor 6.157
2006 Impact Factor 5.889
2005 Impact Factor 5.369
2004 Impact Factor 4.941
2003 Impact Factor 5.201
2002 Impact Factor 4.497
2001 Impact Factor 4.715
2000 Impact Factor 4.579
1999 Impact Factor 4.858
1998 Impact Factor 4.318
1997 Impact Factor 4.105
1996 Impact Factor 3.936
1995 Impact Factor 3.567
1994 Impact Factor 2.78
1993 Impact Factor 2.521
1992 Impact Factor 3.661

Impact factor over time

Impact factor
Year

Additional details

5-year impact 8.17
Cited half-life 6.40
Immediacy index 1.58
Eigenfactor 0.05
Article influence 2.64
Website Neuropsychopharmacology website
Other titles Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
ISSN 1740-634X
OCLC 855449
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Nature Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • Authors retain copyright
    • Published source must be acknowledged and DOI cited
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • On author's personal website and institutional repository
    • If funding agency rules apply, authors may post authors version to their relevant funding body's archive, 6 months after publication
    • This policy is an exception to the default policies of 'Nature Publishing Group'
  • Classification
    yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The central melanocortin (MC) system mediates its effects on food intake via MC3 (MC3R) and MC4 receptors (MC4R). While the role of MC4R in meal size determination, satiation, food preference and motivation is well established, the involvement of MC3R in the modulation of food intake has been less explored. Here, we investigated the role of MC3R on the incentive motivation for food, which is a crucial component of feeding behavior. Dopaminergic neurons within the ventral tegmental area (VTA) play a crucial role in the motivation for food. We here report that MC3Rs are expressed on VTA dopaminergic neurons and that pro-opiomelanocortinergic (POMC) neurons in the arcuate nucleus of the hypothalamus (Arc) innervate these VTA dopaminergic neurons. Our findings show that intracerebroventricular or intra-VTA infusion of the selective MC3R agonist γMSH increases responding for sucrose under a progressive ratio schedule of reinforcement, but not free sucrose consumption in rats. Furthermore, ex-vivo electrophysiological recordings show increased VTA dopaminergic neuronal activity upon γMSH application. Consistent with a dopamine-mediated effect of γMSH, the increased motivation for sucrose after intra-VTA infusion of γMSH was blocked by pretreatment with the dopamine receptor antagonist α-flupenthixol. Taken together, we demonstrate an Arc POMC projection onto VTA dopaminergic neurons that modulates motivation for palatable food via activation of MC3R signaling.Neuropsychopharmacology accepted article preview online, 08 February 2016. doi:10.1038/npp.2016.19.
    No preview · Article · Feb 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Phosphodiesterase 10A (PDE10A) inhibitors are expected to be novel drugs for schizophrenia through activation of both direct and indirect pathway medium spiny neurons. However, excess activation of the direct pathway by a dopamine D1 receptor agonist SKF82958 canceled antipsychotic-like effects of a dopamine D2 receptor antagonist haloperidol in methamphetamine (METH)-induced hyperactivity in rats. Thus, balanced activation of these pathways may be critical for PDE10A inhibitors. Current antipsychotics and the novel PDE10A inhibitor TAK-063, but not the selective PDE10A inhibitor MP-10, produced dose-dependent antipsychotic-like effects in METH-induced hyperactivity and prepulse inhibition in rodents. TAK-063 and MP-10 activated the indirect pathway to a similar extent; however, MP-10 caused greater activation of the direct pathway than did TAK-063. Interestingly, the off-rate of TAK-063 from PDE10A in rat brain sections was faster than that of MP-10, and a slower off-rate PDE10A inhibitor with TAK-063-like chemical structure showed MP-10-like pharmacological profile. In general, faster off-rate enzyme inhibitors are more sensitive than slower off-rate inhibitors to binding inhibition by enzyme substrates. As expected, TAK-063 was more sensitive than MP-10 to binding inhibition by cyclic nucleotides. Moreover, an immunohistochemistry study suggested that cyclic adenosine monophosphate levels in the direct pathway were higher than those in the indirect pathway. These data can explain why TAK-063 showed partial activation of the direct pathway compared to MP-10. The findings presented here suggest that TAK-063's antipsychotic-like efficacy may be attributable to its unique pharmacological properties, resulting in balanced activation of the direct and indirect striatal pathways.Neuropsychopharmacology accepted article preview online, 05 February 2016. doi:10.1038/npp.2016.20.
    No preview · Article · Feb 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: The glutamic acid decarboxylase 1 (GAD1) gene is a major determinant of γ-Aminobutyric acid (GABA), the most abundant inhibitory neurotransmitter modulating local neuronal circuitry. GABAergic dysfunction and expression of GAD1 have been implicated in the pathophysiology of schizophrenia, and in working memory impairment. We examined the influence of the functional GAD1 rs3749034 variant on white matter fractional anisotropy (FA), cortical thickness, and working memory performance in schizophrenia patients and healthy controls (N=197). Using transcranial magnetic stimulation with electroencephalography (TMS-EEG), we subsequently examined the effect of rs3749034 on long-interval cortical inhibition (LICI) in the dorsolateral prefrontal cortex (DLPFC) in schizophrenia patients and healthy controls (N=66). We found that the rs3749034 T-allele carrier risk group had lower voxel-wise FA in prefrontal cortex region (PFWE-corrected<0.05) but not cortical thickness. Mixed-model regression revealed a significant effect on attentional processing and working memory across four performance measures (F1,182=11.5, p=8 × 10(-4)). FA in the prefrontal cortex was associated with digit-span performance. Voxel-wise mediation analysis revealed that the effect GAD1 on poorer digit-span performance statistically predicted the lower white matter FA (PFWE-corrected<0.05). In exploratory analysis, we found a prominent GAD1 genotype-by-diagnosis interaction on DLPFC LICI (F1,56=14.3, p=4.1 × 10(-4)). Our findings converge on variation in GAD1 gene predicting a susceptibility mechanism that affects white matter FA, GABAergic inhibitory neurotransmission in the DLPFC, and working memory performance. Furthermore, via voxel mediation of FA and TMS-EEG intervention, we provide evidence for a potentially causal mechanism through which aberrant DLPFC GABA signaling may contribute to working memory dysfunction.Neuropsychopharmacology accepted article preview online, 29 January 2016. doi:10.1038/npp.2016.14.
    No preview · Article · Jan 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Neuropsychopharmacology, the official publication of the American College of Neuropsychopharmacology, publishing the highest quality original research and advancing our understanding of the brain and behavior.
    No preview · Article · Jan 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: The basal forebrain (BF) cholinergic neurons have long been thought to be involved in behavioral wakefulness and cortical activation. However, owing to the heterogeneity of BF neurons and the poor selectivity of traditional methods, the precise role of BF cholinergic neurons in regulating the sleep-wake cycle remains unclear. We investigated the effects of cell-selective manipulation of BF cholinergic neurons on sleep-wake behavior and electroencephalogram (EEG) power spectrum using pharmacogenetic technique, the 'designer receptors exclusively activated by designer drugs (DREADD)' approach and ChAT-IRES-Cre mice. Our results showed that activation of BF cholinergic neurons expressing hM3Dq receptors significantly and lastingly decreased the EEG delta power spectrum, produced low-delta non-rapid eye movement sleep, and slightly increased wakefulness in both light and dark phases; whereas inhibition of BF cholinergic neurons expressing hM4Di receptors significantly increased EEG delta power spectrum and slightly decreased wakefulness. Next, the projections of BF cholinergic neurons were traced by humanized Renilla green fluorescent protein (hrGFP). Abundant and highly dense hrGFP-positive fibers were observed in the secondary motor cortex and cingulate cortex; and sparse hrGFP-positive fibers were observed in the ventrolateral preoptic nucleus, a known sleep-related structure. Finally, we found that activation of BF cholinergic neurons significantly increased c-Fos expression in the secondary motor cortex and cingulate cortex, but decreased c-Fos expression in the ventrolateral preoptic nucleus. Taken together, these findings reveal that the primary function of BF cholinergic neurons is to inhibit EEG delta activity through the activation of cerebral cortex, rather than to induce behavioral wakefulness.Neuropsychopharmacology accepted article preview online, 22 January 2016. doi:10.1038/npp.2016.13.
    No preview · Article · Jan 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: The nucleus accumbens (NAc) contains a hedonic hotspot in the rostral half of medial shell, where opioid agonist microinjections are known to enhance positive hedonic orofacial reactions to the taste of sucrose ('liking' reactions). Within NAc shell, orexin/hypocretin also has been reported to stimulate food intake and is implicated in reward, whereas blockade of muscarinic acetylcholine receptors by scopolamine suppresses intake and may have anti-reward effects. Here, we show that NAc microinjection of orexin-A in medial shell amplifies the hedonic impact of sucrose taste, but only within the same anatomically rostral site, identical to the opioid hotspot. By comparison, at all sites throughout medial shell, orexin microinjections stimulated 'wanting' to eat, as reflected by increases in intake of palatable sweet chocolates. At NAc shell sites outside the hotspot, orexin selectively enhanced 'wanting' to eat without enhancing sweetness 'liking' reactions. In contrast, microinjections of the antagonist scopolamine at all sites in NAc shell suppressed sucrose 'liking' reactions as well as suppressing intake of palatable food. Conversely, scopolamine increased aversive 'disgust' reactions elicited by bitter quinine at all NAc shell sites. Finally, scopolamine microinjections localized to the caudal half of medial shell additionally generated a fear-related antipredator reaction of defensive treading and burying directed toward the corners of the transparent chamber. Together, these results confirm a rostral hotspot in NAc medial shell as a unique site for orexin induction of hedonic 'liking' enhancement, similar to opioid enhancement. They also reveal distinct roles for orexin and acetylcholine signals in NAc shell for hedonic reactions and motivated behaviors.Neuropsychopharmacology accepted article preview online, 20 January 2016. doi:10.1038/npp.2016.10.
    No preview · Article · Jan 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Poor impulse control is associated with an increased propensity to develop an addiction and may contribute to relapse as high impulsive subjects appear to attribute greater salience toward drug-paired stimuli. In these studies, we determined whether trait impulsivity also predicts the desire to obtain natural reward-paired stimuli. Rats trained on the 5-choice serial reaction time task to measure impulsive action (Experiment 1) or a delay-discounting task to measure impulsive choice (Experiment 2) were separated into low, intermediate, or high impulsive action (L-IA, I-IA, H-IA) or choice (L-IC, I-IC, H-IC) groups. The motivation to obtain a conditioned stimulus (CS) paired with water-reward was subsequently determined by measuring responding for the CS as a conditioned reinforcer (CRf). Dopamine release in the nucleus accumbens (NAc) was also measured using in vivo microdialysis. The effects of amphetamine were assessed on all tests. In Experiment 1, amphetamine increased impulsive action in all groups. L-IA rats initially demonstrated the highest responding for the CRf. Amphetamine increased responding for the CRf and this effect was augmented in L-IA rats. Dopamine release following amphetamine was greatest in L-IA subjects. In Experiment 2, amphetamine increased impulsive choice for L-IC and I-IC rats. However, all groups responded similarly for the CRf and dopamine release was moderately greater in L-IC rats. In conclusion, impulsive choice was unrelated to responding for a CRf. L-IA subjects initially attributed enhanced salience to a CS and exhibited greater dopamine release. Lower dopamine release in H-IA rats could result in reduced reinforcing properties of the CRf.Neuropsychopharmacology accepted article preview online, 19 January 2016. doi:10.1038/npp.2016.9.
    No preview · Article · Jan 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Dopamine is critical for many processes that drive learning and memory, including motivation, prediction error, incentive salience, memory consolidation, and response output. Theories of dopamine's function in these processes have, for the most part, been developed from behavioral approaches that examine learning mechanisms in appetitive tasks. A parallel and growing literature indicates that dopamine signaling is involved in consolidation of memories into stable representations in aversive tasks such as fear conditioning. Relatively little is known about how dopamine may modulate memories that form during extinction, when organisms learn that the relation between previously associated events is severed. We investigated whether fear and reward extinction share common mechanisms that could be enhanced with dopamine D1/5 receptor activation. Pharmacological activation of dopamine D1/5 receptors (with SKF 81297) enhanced extinction of both cued and contextual fear. These effects also occurred in the extinction of cocaine-induced conditioned place preference, suggesting that the observed effects on extinction were not specific to a particular type of procedure (aversive or appetitive). A cAMP/PKA biased D1 agonist (SKF 83959) did not affect fear extinction, whereas a broadly efficacious D1 agonist (SKF 83822) promoted fear extinction. Together, these findings show that dopamine D1/5 receptor activation is a target for the enhancement of fear or reward extinction.Neuropsychopharmacology accepted article preview online, 14 January 2016. doi:10.1038/npp.2016.5.
    No preview · Article · Jan 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: While alcoholism and depression are highly comorbid, treatment options that take this into account are lacking, and mouse models of alcohol (ethanol, EtOH) intake-induced depressive behavior have not been well established. Recent studies utilizing contingent EtOH administration through prolonged two-bottle choice access have demonstrated depression-like behavior following EtOH abstinence in singly-housed female C57BL/6J mice. In the present study, we found that depression-like behavior in the forced swim test (FST) is revealed only after a protracted (2 weeks), but not acute (24 h), abstinence period. No effect on anxiety-like behavior in the EPM was observed. Further, we found that once established, the affective disturbance is long-lasting, as we observed significantly enhanced latencies to approach food even 35 days after ethanol withdrawal in the novelty-suppressed feeding test (NSFT). We were able to reverse affective disturbances measured in the NSFT following EtOH abstinence utilizing the N-methyl D-aspartate receptor (NMDAR) antagonist and antidepressant ketamine, but not memantine, another NMDAR antagonist. Pretreatment with the monoacylglycerol (MAG) lipase inhibitor JZL-184 also reduced affective disturbances in the NSFT in ethanol withdrawn mice, and this effect was prevented by co-administration of the CB1 inverse agonist rimonabant. Endocannabinoid levels were decreased within the BLA during abstinence compared to during drinking. Finally, we demonstrate that the depressive behaviors observed do not require a sucrose fade, and that this drinking paradigm may favor the development of habit-like EtOH consumption. These data could set the stage for developing novel treatment approaches for alcohol-withdrawal-induced mood and anxiety disorders.Neuropsychopharmacology accepted article preview online, 11 January 2016. doi:10.1038/npp.2016.3.
    No preview · Article · Jan 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: There is substantial evidence that NMDA receptor (NMDAR) hypofunction contributes to the pathophysiology of schizophrenia. A recent large-scale genome-wide association study identified serine racemase (SR), the enzyme that produces the NMDAR co-agonist D-serine, as a risk gene for schizophrenia. Serine racemase knockout (SR-/-) mice, which lack D-serine, exhibit many of the neurochemical and behavioral abnormalities observed in schizophrenia. Metabotropic glutamate receptor 5 (mGlu5) positive allosteric modulators (PAMs) are currently being developed to treat cognitive dysfunction. We used in vitro electrophysiology to determine whether the mGlu5 PAM, VU0409551, directly enhances NMDAR function in hippocampal slices from adult male SR-/- mice. We administered VU0409551 systemically for 5 days to adult male wild-type C57BL/6 animals to determine the optimal dose to test in SR-/- mice. We used Western blot analyses and trace-fear conditioning to determine whether 5 days of VU0409551 treatment could reverse the neuroplasticity and learning deficits, respectively, in SR-/- mice. We show that VU0409551 enhances NMDAR function and rescues long-term potentiation (LTP) in hippocampal slices obtained from SR-/- mice. Systemic treatment with VU0409551 (10, 30 mg/kg) causes a dose-dependent increase in the Akt/GS3Kα/β signaling pathway, which is reduced in SR-/- mice and in schizophrenia. Furthermore, administration of VU0409551 to SR-/- mice reverses their deficits in several neuroplasticity signaling pathways and improves their contextual fear memory. These results support positive allosteric modulation of mGlu5, particularly with VU0409551, as a viable mechanism to reverse the deficits in NMDAR function, synaptic plasticity, and memory that are known to be impaired in schizophrenia.Neuropsychopharmacology accepted article preview online, 07 January 2016. doi:10.1038/npp.2016.2.
    No preview · Article · Jan 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Anxiety disorders are debilitating psychiatric illnesses with detrimental effects on human health. These heightened states of arousal are often in the absence of obvious threatening cues and are difficult to treat due to a lack of understanding of the neural circuitry and cellular machinery mediating these conditions. Activation of noradrenergic circuitry in the basolateral amygdala is thought to play a role in stress, fear, and anxiety and the specific cell and receptor types responsible is an active area of investigation. Here we take advantage of two novel cellular approaches to dissect the contributions of G-protein signaling in acute and social anxiety-like states. We used a chemogenetic approach utilizing the Gαs DREADD (rM3Ds) receptor and show that selective activation of generic Gαs signaling is sufficient to induce acute and social anxiety-like behavioral states in mice. Second, we use a recently characterized chimeric receptor composed of rhodopsin and the β2-adrenergic receptor (Opto-β2AR) with in vivo optogenetic techniques to selectively activate Gαs β-adrenergic signaling exclusively within excitatory neurons of the basolateral amygdala. We found that optogenetic induction of β-adrenergic signaling in the basolateral amygdala is sufficient to induce acute and social anxiety-like behavior. These findings support the conclusion that activation of Gαs signaling in the basolateral amygdala plays a role in anxiety. These data also suggest that acute and social anxiety-like states may be mediated through signaling pathways identical to β-adrenergic receptors thus providing support that inhibition of this system may be an effective anxiolytic therapy.Neuropsychopharmacology accepted article preview online, 04 January 2016. doi:10.1038/npp.2015.371.
    No preview · Article · Jan 2016 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Activin, a member of the transforming growth factor-β family, exerts multiple functions in the nervous system. Originally identified as a neurotrophic and -protective agent, increasing evidence implicates activin also in the regulation of glutamatergic and GABAergic neurotransmission in brain regions associated with cognitive and affective functions. To explore how activin impacts on ethanol potentiation of GABA synapses and related behavioral paradigms, we used an established transgenic model of disrupted activin receptor signaling, in which mice express a dominant-negative activin receptor IB mutant (dnActRIB) under the control of the CaMKIIα promoter. Comparison of GABAA receptor currents in hippocampal neurons from dnActRIB mice and wild type mice showed that all concentrations of ethanol tested (30-150 mM) produced much stronger potentiation of phasic inhibition in the mutant preparation. In dentate granule cells of dnActRIB mice, tonic GABA inhibition was more pronounced than in wild type neurons, but remained insensitive to low ethanol (30 mM) in both preparations. The heightened ethanol sensitivity of phasic inhibition in mutant hippocampi resulted from both pre- and postsynaptic mechanisms, the latter probably involving PKCɛ. At the behavioral level, ethanol produced significantly stronger sedation in dnActRIB mice than in wild type mice, but did not affect consumption of ethanol or escalation after withdrawal. We link the abnormal narcotic response of dnActRIB mice to ethanol to the excessive potentiation of inhibitory neurotransmission. Our study suggests that activin counteracts over-sedation from ethanol by curtailing its augmenting effect at GABA synapses.Neuropsychopharmacology accepted article preview online, 31 December 2015. doi:10.1038/npp.2015.372.
    No preview · Article · Dec 2015 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Sex differences in the sensitivity to nicotine may influence vulnerability to tobacco dependence. The goal of this study was to investigate the dose-response function for the reinforcing and subjective effects of intravenous (IV) nicotine in male and female smokers. Tobacco dependent subjects (12 male, 14 female) participated in four experimental sessions in which they received sample infusions of saline and nicotine (0.1, 0.2, 0.3 or 0.4 mg doses) in a randomized double-blind cross-over design. During each session, subjects first received the sample infusions and heart rate, blood pressure and subjective stimulatory, pleasurable and aversive responses were monitored. Immediately following the sample infusions, subjects self-administered either nicotine or saline in six double-blind forced-choice trials. A sex by dose interaction was observed in the nicotine choice paradigm. Nicotine self-administration rate was negatively correlated with nicotine dose in males (males displayed choice preference for low doses of nicotine over high doses of nicotine), but no significant relationship between dose and choice preference was evident in females. Relative to placebo, sample doses of nicotine increased heart rate and blood pressure and induced stimulatory, pleasurable and aversive subjective effects. Diastolic blood pressure increased dose-dependently in males, but not in females. These findings, which demonstrate sex differences in nicotine self-administration for doses that are near to the reinforcement threshold, suggest that male and female smokers may respond differently to changes in nicotine doses available for self-administration.Neuropsychopharmacology accepted article preview online, 31 December 2015. doi:10.1038/npp.2015.373.
    No preview · Article · Dec 2015 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cannabidiol (CBD), a constituent of cannabis with few psychoactive effects, has been reported in some studies to attenuate certain aspects of Δ(9)-tetrahydrocannabinol (THC) intoxication. However, most studies have tested only one dose of CBD in combination with one dose of oral THC making it difficult to assess the nature of this interaction. Further, the effect of oral CBD on smoked cannabis administration is unknown. The objective of this multi-site, randomized, double-blind, within-subject laboratory study was to assess the influence of CBD (0, 200, 400, 800 mg, p.o.) pretreatment on the reinforcing, subjective, cognitive, and physiological effects of smoked cannabis [0.01 (inactive), 5.30-5.80% THC]. Non-treatment-seeking, healthy cannabis smokers (n=31; 17M,14F) completed 8 outpatient sessions. CBD was administered 90 min prior to cannabis administration. The behavioral and cardiovascular effects of cannabis were measured at baseline and repeatedly throughout the session. A subset of participants (n=8) completed an additional session to measure plasma CBD concentrations after administration of the highest CBD dose (800 mg). Under placebo CBD conditions, active cannabis (1) was self-administered by significantly more participants than placebo cannabis, and (2) produced significant, time-dependent increases in ratings of 'High,' 'Good Effect,' ratings of the cannabis cigarette (eg, strength, liking) and heart rate relative to inactive cannabis. CBD, which alone produced no significant psychoactive or cardiovascular effects, did not significantly alter any of these outcomes. Cannabis self-administration, subjective effects, and cannabis ratings did not vary as a function of CBD dose relative to placebo capsules. These findings suggest that oral CBD does not reduce the reinforcing, physiological or positive subjective effects of smoked cannabis.Neuropsychopharmacology accepted article preview online, 28 December 2015. doi:10.1038/npp.2015.367.
    No preview · Article · Dec 2015 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology