GABA mediaties the inhibitory effect of lateral amygdaloid nucleus stimulation on the acoustic response of neurons in A I cortex: An in vivo microiontophoretic study.
- Author:
De-Fu HE
1
;
Fu-Jun CHEN
;
Shao-Ci ZHOU
Author Information
1. Department of Environmental Science and Brain Science Research Center, East China Normal University, Shanghai 200062, China. defuhe@citiz.net
- Publication Type:Journal Article
- MeSH:
Acoustic Stimulation;
Amygdala;
physiology;
Animals;
Baclofen;
pharmacology;
Bicuculline;
pharmacology;
Cerebral Cortex;
physiology;
Electric Stimulation;
Evoked Potentials, Auditory;
physiology;
GABA Agonists;
pharmacology;
GABA Antagonists;
pharmacology;
Iontophoresis;
methods;
Male;
Microelectrodes;
Neurons;
physiology;
Rats;
Rats, Sprague-Dawley;
Receptors, GABA-A;
physiology;
gamma-Aminobutyric Acid;
physiology
- From:
Acta Physiologica Sinica
2004;56(3):374-378
- CountryChina
- Language:English
-
Abstract:
Experiments were performed on Sprague Dawley rats with multibarrel microelectrode technique. The effects of acoustic response of A I cortex neurons produced by electrical stimulation of lateral amygdaloid nucleus (LA) and the influence of GABA were observed. Experimental results showed that iontophoretic administration of GABA caused a pronounced inhibition of the electrical activity of A-I neurons. Blockade of GABA(A) with bicuculline (BIC) facilitated the acoustic response. The acoustic response of A-I neurons was inhibited when the LA was stimulated. Iontophoretic application of GABA resulted in a similar inhibitory effect as that of LA stimulation. Blockade of GABA(A) with bicuculline reversed the inhibitory effect of LA stimulation on the acoustic response of A-I neurons. In contrast, application of strychnine, a glycine receptor antagonist, could not reverse the inhibitory effect of LA. Baclofen, a GABA(B) agonist, did not affect the acoustic response of the auditory neurons. These results indicate that GABA is the ultimate transmitter which mediates the LA stimulation-induced inhibition of the acoustic response of A-I neurons in rats, possibly via the GABA(A) receptor.
