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首页> 外文期刊>Neuron >Differences in cortical versus subcortical GABAergic signaling: a candidate mechanism of electroclinical uncoupling of neonatal seizures.
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Differences in cortical versus subcortical GABAergic signaling: a candidate mechanism of electroclinical uncoupling of neonatal seizures.

机译：皮层和皮层下GABA能信号的差异：新生儿癫痫发作的电临床解偶联的候选机制。

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摘要

Electroclinical uncoupling of neonatal seizures refers to electrographic seizure activity that is not clinically manifest. Uncoupling increases after treatment with Phenobarbital, which enhances the GABA(A) receptor (GABA(A)R) conductance. The effects of GABA(A)R activation depend on the intracellular Cl(-) concentration ([Cl(-)](i)) that is determined by the inward Cl(-) transporter NKCC1 and the outward Cl(-) transporter KCC2. Differential maturation of Cl(-) transport observed in cortical versus subcortical regions should alter the efficacy of GABA-mediated inhibition. In perinatal rat pups, most thalamic neurons maintained low [Cl(-)](i) and were inhibited by GABA. Phenobarbital suppressed thalamic seizure activity. Most neocortical neurons maintained higher [Cl(-)](i), and were excited by GABA(A)R activation. Phenobarbital had insignificant anticonvulsant responses in the neocortex until NKCC1 was blocked. Regional differences in the ontogeny of Cl(-) transport may thus explain why seizure activity in the cortex is not suppressed by anticonvulsants that block the transmission of seizure activity through subcortical networks.
机译：新生儿癫痫发作的电临床解偶联是指临床上未表现出的电描记性癫痫发作活动。苯巴比妥治疗后，解偶联增加，从而增强了GABA（A）受体（GABA（A）R）的电导率。 GABA（A）R激活的影响取决于细胞内Cl（-）浓度（[Cl（-）]（i）），该浓度由向内Cl（-）转运蛋白NKCC1和向外Cl（-）转运蛋白KCC2确定。在皮层和皮层下区域观察到的Cl（-）转运差异成熟应改变GABA介导的抑制作用。在围产期大鼠幼崽中，大多数丘脑神经元维持低[Cl（-）]（i）并被GABA抑制。苯巴比妥抑制丘脑癫痫发作活动。大多数新皮质神经元维持较高的[Cl（-）]（i），并受到GABA（A）R激活的兴奋。苯巴比妥在新皮层中没有明显的抗惊厥反应，直到NKCC1被阻断。 Cl（-）转运的个体发育的区域差异因此可以解释为什么抗惊厥药不能抑制皮质中的癫痫发作活动，因为抗惊厥药会阻止癫痫活动通过皮层下网络传播。

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