http://www.cnr.it/ontology/cnr/individuo/prodotto/ID37800

Gamma-Hydroxybutyric acid (GHB) and the mesoaccumbens reward circuit: evidence for GABAB receptor mediated effects. (Articolo in rivista)

Type

Prodotto della ricerca (Classe)
Articolo in rivista (Classe)

Label

Gamma-Hydroxybutyric acid (GHB) and the mesoaccumbens reward circuit: evidence for GABAB receptor mediated effects. (Articolo in rivista) (literal)

Anno

2005-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.1016/j.neuroscience.2004.11.021 (literal)

Alternative label

Pistis M., Muntoni A.L., Pillolla G., Perra S., Cignarella G., Melis M. , Gessa G.L (2005)
Gamma-Hydroxybutyric acid (GHB) and the mesoaccumbens reward circuit: evidence for GABAB receptor mediated effects.
in Neuroscience
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Pistis M., Muntoni A.L., Pillolla G., Perra S., Cignarella G., Melis M. , Gessa G.L (literal)

Pagina inizio

465 (literal)

Pagina fine

474 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

131 (literal)

Rivista

Neuroscience (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali

10 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

2 (literal)

Note

PubMe (literal)
ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

(1) B. B. Brodie Department of Neuroscience, University of Cagliari, Monserrato, Italy; (2) CNR Institute of Neuroscience-Section of Cagliari, University of Cagliari, Monserrato, Italy; (3) Center of Excellence \"Neurobiology of Addiction\", University of Cagliari, Monserrato, Italy; (4) Institute of Pharmaceutical and Toxicological Chemistry, University of Milan, Milan, Italy (literal)

Titolo

Gamma-Hydroxybutyric acid (GHB) and the mesoaccumbens reward circuit: evidence for GABAB receptor mediated effects. (literal)

Abstract

Gamma-hydroxybutyric acid (GHB) is a short-chain fatty acid naturally occurring in the mammalian brain, which recently emerged as a major recreational drug of abuse. GHB has multiple neuronal mechanisms including activation of both the GABA(B) receptor, and a distinct GHB-specific receptor. This complex GHB-GABA(B) receptor interaction is probably responsible for the multifaceted pharmacological, behavioral and toxicological profile of GHB. Drugs of abuse exert remarkably similar effects upon reward-related circuits, in particular the mesolimbic dopaminergic system and the nucleus accumbens (NAc). We used single unit recordings in vivo from urethane-anesthetized rats to characterize the effects of GHB on evoked firing in NAc \"shell\" neurons and on spontaneous activity of antidromically identified dopamine (DA) cells located in the ventral tegmental area. GHB was studied in comparison with the GABA(B) receptor agonist baclofen and antagonist (2S)(+)-5,5-dimethyl-2-morpholineacetic acid (SCH50911). Additionally, we utilized a GHB analog, gamma-(p-methoxybenzil)-gamma-hydroxybutyric acid (NCS-435), devoid of GABA(B) binding properties, but with high affinity for specific GHB binding sites. In common with other drugs of abuse, GHB depressed firing in NAc neurons evoked by the stimulation of the basolateral amygdala. On DA neurons, GHB exerted heterogeneous effects, which were correlated to the baseline firing rate of the cells but led to a moderate stimulation of the DA system. All GHB actions were mediated by GABA(B) receptors, since they were blocked by SCH50911 and were not mimicked by NCS-435. Our study indicates that the electrophysiological profile of GHB is close to typical drugs of abuse: both inhibition of NAc neurons and moderate to strong stimulation of DA transmission are distinctive features of diverse classes of abused drugs. Moreover, it is concluded that addictive and rewarding properties of GHB do not necessarily involve a putative high affinity GHB receptor. (literal)

Prodotto di