GABA(A) and GABA(B) receptors differentially regulate synaptic transmission in the auditory thalamo-amygdala pathway: An in vivo microiontophoretic study and a model

Stimulation of the medial geniculate body elicits extracellular single unit responses in the lateral nucleus of the amygdala that are dependent upon glutamatergic neurotransmission [Li et al. (1995) Exp. Brain Res., 105:87- 100]. In the present study, we examined the contribution of inhibitory amine acid transmission to these excitatory responses. Antagonists of GABA(A) or GABA(B) receptors were delivered microiontophoretically to cells activated by stimulation of the medial geniculate body. Blockade of GABA(A) receptors with bicuculline resulted in a pronounced increase in evoked short latency unit responses (4-8 ms). In some cases, cells that were not responsive to the stimulation became responsive in the presence of bicuculline. In contrast, delivery of GABA(B) antagonists, Phaclofen or 2-OH-saclofen, did not affect these short-latency responses. Using paired-pulse stimulation, both short (<30 ms) and longer (>50 ms) latency inhibitory processes were revealed. GABA(A) blockade eliminated the short latency inhibition and GABA(B) blockade eliminated the longer latency inhibition in most cells. These results suggest that the activation of GABA(A) and GABA(B) receptors differentially regulate glutamatergic synaptic transmission in the auditory thalamo-amygdala pathway. Moreover, our findings suggest that at least part of this regulation is via a feedforward mechanism. We tested the sufficiency of feedforward inhibition to account for the data using a simple computational model that incorporates the results presented here.