Lee Seungho, Kim Joung-Hun
Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang 37673, Korea.
Exp Neurobiol. 2019 Jun;28(3):320-328. doi: 10.5607/en.2019.28.3.320. Epub 2019 Jun 26.
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.
基底外侧杏仁核(BLA)接受来自基底前脑胆碱能神经元的密集投射。乙酰胆碱可促成杏仁核依赖的行为:恐惧记忆的形成与消退以及奖赏性工具性学习。然而,在回路水平上的胆碱能机制尚未明确。我们证明,胆碱能诱导的BLA锥体神经元双突触抑制呈现出一种逆行形式的短期突触抑制,即去极化诱导的抑制性抑制(DSI)。烟碱受体的激活足以在胆囊收缩素(CCK)阳性抑制性神经元中引发动作电位,这些神经元通过其胞体周围突触强烈抑制锥体神经元。我们的细胞类型特异性单突触逆行追踪还显示,CCK神经元接受基底前脑胆碱能神经元的支配。因此,我们的数据表明,CCK抑制性神经元介导了胆碱能诱导的BLA锥体神经元双突触抑制。