Ethanol potentiates GABAergic synaptic transmission in a postsynaptic neuron/synaptic bouton preparation from basolateral amygdala.
J Neurophysiol
; 96(1): 433-41, 2006 Jul.
Article
em En
| MEDLINE
| ID: mdl-16624993
ABSTRACT
Interactions between ethanol and synaptic transmission mediated by gamma -amino-N-butyric acid (GABA) have been suggested to contribute to alcohol intoxication. Ethanol effects on postsynaptic GABAA receptors have been the major focus of this line of research. There is increasing evidence that ethanol potentiation of GABAergic transmission involves increased GABA release from presynaptic terminals. In the present study, a mechanically isolated neuron/bouton preparation from the basolateral amygdala was used to examine the effects of ethanol on spontaneous GABAergic synaptic currents elicited by GABA release from the presynaptic terminals. We found that ethanol application produced a rapid increase in the frequency of spontaneous GABAergic synaptic currents. An acute tolerance to ethanol was also observed, and this tolerance involved GABAB receptor activation. The ethanol-induced potentiation did not involve alterations in the function of postsynaptic GABAA receptors and was independent of presynaptic action potential firing. These findings indicate that ethanol potentiates GABA release, most likely via a direct action on presynaptic boutons.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Depressores do Sistema Nervoso Central
/
Terminações Pré-Sinápticas
/
Transmissão Sináptica
/
Etanol
/
Ácido gama-Aminobutírico
/
Tonsila do Cerebelo
/
Neurônios
Limite:
Animals
Idioma:
En
Revista:
J Neurophysiol
Ano de publicação:
2006
Tipo de documento:
Article
País de afiliação:
Estados Unidos