ArticleNeuroscience research2016
Distinct neuronal activation patterns are associated with PCP-induced social withdrawal and its reversal by the endocannabinoid-enhancing drug URB597.
Article in Neuroscience research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Multidimensional analysis of social withdrawal in the sub-chronic phencyclidine rat model for schizophrenia.Psychopharmacology · 2026Article
- Cocaine-induced loss of LTD and social impairments are restored by fatty acid amide hydrolase inhibition.Scientific reports · 2023Article
- Inhibitors of Endocannabinoids' Enzymatic Degradation as a Potential Target of the Memory Disturbances in an Acute N-Methyl-D-Aspartate (NMDA) Receptor Hypofunction Model of Schizophrenia in Mice.International journal of molecular sciences · 2023Article
- Endocannabinoid metabolism inhibition has no effect on spontaneous fear recovery or extinction resistance in Lister hooded rats.Frontiers in pharmacology · 2022Article
- URB597 induces subtle changes to aggression in adult Lister Hooded rats.Frontiers in psychiatry · 2022Article
- From the Clinic to the Laboratory, and Back Again: Investigations on Cannabinoids and Endocannabinoid System Modulators for Treating Schizophrenia.Frontiers in psychiatry · 2021Review
- Differential effects of Δ9-tetrahydrocannabinol dosing on correlates of schizophrenia in the sub-chronic PCP rat model.PloS one · 2020Article
- Kynurenines and the Endocannabinoid System in Schizophrenia: Common Points and Potential Interactions.Molecules (Basel, Switzerland) · 2019Review
- Endocannabinoid Signaling in the Control of Social Behavior.Trends in neurosciences · 2017Review
- The endocannabinoid system in social anxiety disorder: from pathophysiology to novel therapeutics.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999)Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The fatty acid amide hydrolase inhibitor, URB597, an endocannabinoid enhancing drug, reverses social withdrawal in the sub-chronic PCP rat model of schizophrenia, but reduces social interaction (SI) in controls. To identify the anatomical substrates associated with PCP-induced social withdrawal and the contrasting effects of URB597 on SI in PCP- versus saline-treated rats, we analyzed SI-induced c-Fos expression in 28 brain areas relevant to schizophrenia and/or social behavior following vehicle or URB597 administration. In saline-treated rats, SI was accompanied by changes in c-Fos expression in the infralimbic and orbitofrontal cortices, dorsomedial caudate putamen, ventrolateral nucleus of the septum, dorsolateral periaqueductal gray (dlPAG) and central amygdala. Except for the dlPAG, these changes were not observed in PCP-treated rats or in saline-treated rats receiving URB597. In the dorsomedial part of the bed nucleus of the stria terminalis (dmBNST), SI-induced c-Fos expression was observed only in PCP-treated rats. Interestingly, URB597 in PCP-treated rats restored a similar c-Fos expression pattern as observed in saline-treated rats: activation of the orbitofrontal cortex, inhibition of the central amygdala and suppression of activation of the dmBNST. These data suggest that orbitofrontal cortex, central amygdala and dmBNST play a critical role in the reversal of PCP-induced social withdrawal by URB597.
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