Evidence for the perirhinal cortex as a requisite component in the seizure network following seizure repetition in an inherited form of generalized clonic seizures.
Evidence for the perirhinal cortex as a requisite component in the seizure network following seizure repetition in an inherited form of generalized clonic seizures.
复制标题
有证据表明，在遗传性全身阵挛性癫痫发作重复发作后，鼻周皮层是癫痫网络中必要的组成部分。
DOI：
10.1016/j.brainres.2005.04.070
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发表时间：
2005
期刊：
影响因子：
2.9
通讯作者：
Faingold,CarlL
中科院分区：
文献类型：
--
作者：
Raisinghani,Manish;Faingold,CarlL
嗅周皮层（PRh）是强烈牵连的神经网络subserving前脑驱动的部分发作癫痫发作，但是否PRh在全身发作癫痫发作中发挥作用尚不清楚。遗传性癫痫易感大鼠（GEPR-3s）的中度癫痫发作严重度亚系表现出全身性发作的阵挛性听源性癫痫发作（AGS），但在重复性AGS（AGS点燃）之后，在全身性阵挛之后立即出现另外的行为，面部和前肢（F&F）阵挛。F&F阵挛被认为是由前脑结构驱动的。本体内研究使用PRh局灶性阻断或细胞外PRh神经元记录，同时进行行为观察，以检查PRh在GEPR-3s中AGS点燃前后AGS神经元网络中所起的作用。双侧PRh内微量注射NMDA受体拮抗剂[2-amino-7-phosphonoheptanoic acid，AP 7（0.2-7.5 nmol/侧）]对AGS点燃前后的全身阵挛无影响。然而，完全和可逆的封锁，只有F&F阵挛发作行为诱导的AP 7（1和7.5 nmol）在AGS-kindled GEPR-3。AGS点燃后PRh神经元对声刺激的反应显著增加。紧张性PRh神经元放电模式出现在全身阵挛前后AGS点燃。在F&F阵挛期间，PRh神经元出现爆发性放电，这是兴奋性增加的指标。这些神经生理学和显微注射研究结果支持PRh在AGS点燃诱导的惊厥行为中的关键作用。这些数据是第一个迹象表明，PRh参与重要的AGS的神经网络作为AGS点燃的结果，并证明了以前未知的参与PRh全身发作癫痫发作。
Perirhinal cortex (PRh) is strongly implicated in neuronal networks subserving forebrain-driven partial onset seizures, but whether PRh plays a role in generalized onset seizures is unclear. The moderate seizure severity substrain of genetically epilepsy-prone rats (GEPR-3s) exhibits generalized onset clonic audiogenic seizures (AGS), but following repetitive AGS (AGS kindling), an additional behavior, facial and forelimb (F&F) clonus emerges immediately following generalized clonus. F&F clonus is thought to be driven from forebrain structures. The present in vivo study used PRh focal blockade or extracellular PRh neuronal recording with simultaneous behavioral observations to examine the role played by PRh in AGS neuronal networks before and after AGS kindling in GEPR-3s. Bilateral microinjection of an NMDA receptor antagonist [2-amino-7-phosphonoheptanoic acid, AP7 (0.2–7.5 nmol/side)] into PRh did not affect generalized clonus before or after AGS kindling. However, complete and reversible blockade of only the F&F clonic seizure behavior was induced by AP7 (1 and 7.5 nmol) in AGS-kindled GEPR-3s. Significant increases in PRh neuronal responses to acoustic stimuli occurred after AGS kindling. Tonic PRh neuronal firing patterns appeared during generalized clonus before and after AGS kindling. During F&F clonus, burst firing, an indicator of increased excitability, appeared in PRh neurons. These neurophysiological and microinjection findings support a critical role of PRh in generation of this AGS kindling-induced convulsive behavior. These data are the first indication that PRh participates importantly in the neuronal network for AGS as a result of AGS kindling and demonstrate a previously unknown involvement of PRh in generalized onset seizures.