皮层GABA受体诱导的失神发作

CORTICAL GABA RECEPTORS INDUCE ABSENCE SEIZURES

利用生物物理平均场模型,通过在皮层引人慢抑制性中间神经元集群,发现抑制性受体GABAa和GABAb在通路抑制性中间神经元集群(IIN)-兴奋性锥体神经元集群(EPN)中均参与了失神发作的调控。特别地,棘慢波放电(SWDs)的出现与一个尺度因子K有关,其被定义为受体GABAa和GABAb的相对强度;由于GABAb受体的慢动力学也是一个致痫因子,因此通过尺度因子K和GABAb时滞t2的状态分析,发现它们可以共同诱导失神发作。这些结果对GABA受体如何诱导失神发作提供了理论指导,并可能为这种脑部疾病的治疗提供新的见解。

Based on a biophysical mean-field model,slow inhibitory intemeuron population was introduced into the cortex to study absence seizures induced by cortical GABA receptors,it was found that inhibitory receptors GABAa and GABAb in pathway inhibitory intemeuron population(IIN)-excitatory pyramidal neuronal population(EPN)both participate in the control of absence seizures through introducing slow IIN.Especially,the appearance of spike and wave discharges(SWDs)is related to a scale factor K,which is defined as the relative strength of the receptors GABAa and GABAb.In addition,the slow kinetics of GABAb receptors is also a pathologic factor.Therefore,through the state analysis of scale factor K and the GABAb delay,it was found that they can jointly induce the absence seizures.These results provide a theoretical guidance on how the GABA receptors induce absence seizures,and may provide new insights into the treatment of this brain disease.