谷氨酸的
神经科学
基底外侧杏仁核
扁桃形结构
医学
加巴能
颞叶
终纹
红藻氨酸
癫痫
内科学
谷氨酸受体
生物
抑制性突触后电位
受体
作者
Yan‐Hui Sun,Bin Hu,Li‐Heng Tan,Lin Lin,Shuxia Cao,Tony Wu,Hao Wang,Bin Yu,Qin Wang,Hong Lian,Jiadong Chen,Xiao‐Ming Li
标识
DOI:10.1002/advs.202407525
摘要
Abstract The amygdaloid complex consists of multiple nuclei and is a key node in controlling temporal lobe epilepsy (TLE) in both human and animal model studies. However, the specific nucleus in the amygdaloid complex and the neural circuitry governing seizures remain unknown. Here, it is discovered that activation of glutamatergic neurons in the posterior basolateral amygdala (pBLA) induces severe seizures and even mortality. The pBLA glutamatergic neurons project collateral connections to multiple brain regions, including the insular cortex (IC), bed nucleus of the stria terminalis (BNST), and central amygdala (CeA). Stimulation of pBLA‐targeted IC neurons triggers seizures, whereas ablation of IC neurons suppresses seizures induced by activating pBLA glutamatergic neurons. GABAergic neurons in the BNST and CeA establish feedback inhibition on pBLA glutamatergic neurons. Deleting GABAergic neurons in the BNST or CeA leads to sporadic seizures, highlighting their role in balancing pBLA activity. Furthermore, pBLA neurons receive glutamatergic inputs from the ventral hippocampal CA1 (vCA1). Ablation of pBLA glutamatergic neurons mitigates both acute and chronic seizures in the intrahippocampal kainic acid‐induced mouse model of TLE. Together, these findings identify the pBLA as a pivotal nucleus in the amygdaloid complex for regulating epileptic seizures in TLE.
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