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CB cannabinoid receptor-mediated anandamide signalling reduces the defensive behaviour evoked through GABA receptor blockade in the dorsomedial division of the ventromedial hypothalamus. | LitMetric

CB cannabinoid receptor-mediated anandamide signalling reduces the defensive behaviour evoked through GABA receptor blockade in the dorsomedial division of the ventromedial hypothalamus.

Neuropharmacology

Laboratory of Neuroanatomy and Neuropsychobiology, Department of Pharmacology, Ribeirão Preto Medical School of the University of São Paulo (USP), Av. Bandeirantes 3900, Ribeirão Preto, São Paulo, 14049-900, Brazil; NAP-USP-Neurobiology of Emotions (NuPNE) Research Centre, FMRP-USP, Ribeirão Preto, São Paulo, Brazil. Electronic address:

Published: February 2017

AI Article Synopsis

  • The study investigates how cannabinoids, particularly in the hypothalamus, affect behaviors linked to fear and panic, especially after reducing GABA activity.
  • Researchers focused on the dorsomedial division of the ventromedial hypothalamus (VMHdm) and used anandamide (AEA) to examine its role in modulating defensive responses triggered by GABA receptor blockade with bicuculline.
  • Results showed that AEA at a specific dose reduced defense behaviors induced by bicuculline, but this effect was blocked by a CB receptor antagonist, indicating a complex interaction between endocannabinoids and cannabinoid receptors in regulating fear responses.

Article Abstract

The effects of cannabinoids in brain areas expressing cannabinoid receptors, such as hypothalamic nuclei, are not yet well known. Several studies have demonstrated the role of hypothalamic nuclei in the organisation of behavioural responses induced through innate fear and panic attacks. Panic-prone states are experimentally induced in laboratory animals through a reduction in the GABAergic activity. The aim of the present study was to examine panic-like elaborated defensive behaviour evoked by GABA receptor blockade with bicuculline (BIC) in the dorsomedial division of the ventromedial hypothalamus (VMHdm). We also aimed to characterise the involvement of endocannabinoids and the CB cannabinoid receptor in the modulation of elaborated defence behavioural responses organised with the VMHdm. The guide-cannula was stereotaxicaly implanted in VMHdm and the animals were treated with anandamide (AEA) at different doses, and the effective dose was used after the pre-treatment with the CB receptor antagonist AM251, followed by GABA receptor blockade in VMHdm. The results showed that the intra-hypothalamic administration of AEA at an intermediate dose (5 pmol) attenuated defence responses induced through the intra-VMHdm microinjection of bicuculline (40 ng). This effect, however, was inhibited when applied central microinjection of the CB receptor antagonist AM251 in the VMHdm. Moreover, AM251 potentiates de non-oriented escape induced by bicuculline, effect blocked by pre-treatment with the TRPV channel antagonist 6-I-CPS. These results indicate that AEA modulates the pro-aversive effects of intra-VMHdm-bicuculline treatment, recruiting CB cannabinoid receptors and the TRPV1 channel is involved in the AM251-related potentiation of bicuculline effects on non-oriented escape behaviour.

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Source
http://dx.doi.org/10.1016/j.neuropharm.2016.04.003DOI Listing

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