Wallenstein G V
Program in Complex Systems and Brain Sciences, Florida Atlantic University, Boca Raton 33431.
Neuroreport. 1994 Jun 27;5(11):1409-12.
Recent studies have suggested that 7-14 Hz spindle rhythms which appear during slow wave sleep and the 3 Hz spike-wave discharge accompanying petit mal seizures share common thalamocortical circuitry. A computational model was used to investigate the manner in which differential changes in the synaptic currents, IGABAA and IGABAB, observed in these cells can transform normal sleep spindles into the pathological oscillations recorded in primate exhibiting generalized petit mal epilepsy. The model suggests that inhibition by GABAergic interneurons and possibly nucleus reticularis thalami cells which reduce IGABA, increases the amplitude of the slower IGABAB. These events produce an extended inhibitory period in relay cells and also lead to the exaggerated post-inhibitory rebound Ca(2+)-dependent burst observed during seizures.
最近的研究表明，慢波睡眠期间出现的7-14赫兹纺锤波节律以及伴有失神小发作的3赫兹棘波放电共享共同的丘脑皮质环路。使用一个计算模型来研究在这些细胞中观察到的突触电流IGABAA和IGABAB的差异变化能够将正常睡眠纺锤波转变为在患有全身性失神癫痫的灵长类动物中记录到的病理性振荡的方式。该模型表明，GABA能中间神经元以及可能的丘脑网状核细胞的抑制作用（其降低了IGABA）增加了较慢的IGABAB的幅度。这些事件在中继细胞中产生了延长的抑制期，并且还导致了在癫痫发作期间观察到的抑制后反弹Ca(2+)依赖性爆发的夸张现象。
