Presynaptic GABAA Receptors Modulate Thalamocortical Inputs in Layer 4 of Rat V1

Fast inhibitory GABAergic transmission plays a fundamental role in neural circuits. Current theories of cortical function assume that fast GABAergic inhibition acts via GABA(A) receptors on postsynaptic neurons, while presynaptic effects of GABA depend on GABA(B) receptor activation. Manipulations of GABA(A) receptor activity in vivo produced different effects on cortical function, which were generally ascribed to the mode of action of a drug, more than its site of action. Here we show that in rodent primary visual cortex, 4-containing GABA(A) receptors can be located on subsets of glutamatergic and GABAergic presynaptic terminals and decrease synaptic transmission. Our data provide a novel mechanistic insight into the effects of changes in cortical inhibition; the ability to modulate inputs onto cortical circuits locally, via presynaptic regulation of release by GABA(A) receptors.