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首页> 外文期刊>The European Journal of Neuroscience >Functional contribution of specific brain areas to absence seizures: role of thalamic gap-junctional coupling.
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Functional contribution of specific brain areas to absence seizures: role of thalamic gap-junctional coupling.

机译：特定大脑区域对癫痫发作的功能性贡献：丘脑间隙-结点耦合的作用。

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摘要

The synchronized discharges typical of seizures have a multifactorial origin at molecular, cellular and network levels. During recent years, the functional role of gap-junctional coupling has received increased attention as a mechanism that may participate in seizure generation. We have investigated the possible functional roles of thalamic and hippocampal gap-junctional communication (GJC) in the generation of spike-and-wave discharges in a rodent model of atypical absence seizures. Seizures in this model spread throughout limbic, thalamic and neocortical areas. Rats were chronically implanted with cannulae to deliver drugs or saline, and local field potentials recordings were performed using intracerebral electrodes positioned in distinct brain areas. Initially, the effects on synaptic transmission of the gap-junctional blockers used in this study were determined. Neither carbenoxolone (CBX) nor 18-alpha-glycyrrhetinic acid altered chemical synaptic transmission at the concentrations tested. These two compounds, when injected via cannulae into the reticular nucleus of the thalamus (NRT), decreased significantly the duration of seizures as compared with saline injections or injections of the CBX inactive derivative glycyrrhizic acid. CBX injections into the hippocampus resulted in diminished seizure activity as well. NRT injections of trimethylamine, which presumably causes intracellular alkalinization (thereby promoting gap-junctional opening), enhanced seizures and spindle activity. These observations suggest that, in this rodent model, thalamic and limbic areas are involved in the synchronous paroxysmal activity and that GJC contributes to the spike-and-wave discharges.
机译：癫痫发作的典型同步放电在分子，细胞和网络水平上具有多因素起源。近年来，间隙连接连接的功能作用作为一种可能参与癫痫发作的机制而受到越来越多的关注。我们研究了在非典型性癫痫发作的啮齿动物模型中，丘脑和海马间隙连接通讯（GJC）在产生波峰放电中的可能功能作用。该模型中的癫痫发作遍布边缘，丘脑和新皮层区域。将大鼠长期植入插管以输送药物或盐水，并使用位于不同大脑区域的脑内电极进行局部场电位记录。最初，确定了本研究中使用的间隙连接阻滞剂对突触传递的影响。在所测试的浓度下，羧苄索龙（CBX）和18-α-甘草次酸均未改变化学突触传递。与盐水注射液或CBX非活性衍生物甘草酸注射液相比，这两种化合物通过插管注射入丘脑网状核（NRT）时，癫痫发作的持续时间明显缩短。向海马注射CBX也会导致癫痫发作活动减少。 NRT注射三甲胺可能会引起细胞内碱化（从而促进缝隙连接处打开），增强癫痫发作和纺锤体活动。这些观察结果表明，在这种啮齿动物模型中，丘脑和边缘区参与了同步的阵发性活动，GJC促进了尖峰和波浪放电。

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