Exp Neurobiol 2019; 28(3): 320-328
Published online June 26, 2019
© The Korean Society for Brain and Neural Sciences
Seungho Lee, and Joung-Hun Kim*
Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang 37673, Korea.
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-54-279-2347, FAX: 82-54-279-5969
The basolateral amygdala (BLA) receives dense projections from cholinergic neurons of the basal forebrain. Acetylcholine can contributes to amygdala-dependent behaviors: formation and extinction of fear memory and appetitive instrumental learning. However, the cholinergic mechanism at the circuit level has not been defined yet. We demonstrated that cholinergic-induced di-synaptic inhibition of BLA pyramidal neurons exhibits a retrograde form of short-term synaptic inhibition, depolarization-induced suppression of inhibition (DSI). Activation of nicotinic receptors was sufficient to evoke action potentials in cholecystokinin (CCK)-positive inhibitory neurons, which strongly inhibit pyramidal neurons through their perisomatic synapses. Our cell type-specific monosynaptic retrograde tracing also revealed that CCK neurons are innervated by basal forebrain cholinergic neurons. Therefore, our data indicated that CCK inhibitory neurons mediate the cholinergic-induced di-synaptic inhibition of BLA pyramidal neurons.