Magnesium (Mg2+) is an essential mineral for several cellular functions. The concentration of this ion below the physiological concentration induces recurrent neuronal discharges both in slices of the hippocampus and in neuronal cultures. These epileptiform discharges are initially sensitive to the application of N-methyl-D-aspartate (NMDA) receptor antagonists, but these antagonists may lose their effectiveness with prolonged exposure to low [Mg2+], when extracellular Ca2+ reduction occurs, typical of ictal periods, indicating the absence of synaptic connections. The study herein presented aimed at investigating the effect of reducing the [Mg2+] during the induction of Nonsynaptic Epileptiform Activities (NSEA). As an experimental protocol, NSEA were induced in rat hippocampal dentate gyrus (DG), using a bath solution containing high-K+ and zero-added-Ca2+. Additionally, computer simulations were performed using a mathematical model that represents electrochemical characteristics of the tissue of the DG granular layer. The experimental results show that the reduction of [Mg2+] causes an increase in the duration of the ictal period and a reduction in the interictal period, intensifying epileptiform discharges. The computer simulations suggest that the reduction of the Mg2+ level intensifies the epileptiform discharges by a joint effect of reducing the surface charge screening and reducing the activity of the Na/K pump.

中文翻译：

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非突触模型中低镁浓度对发作期放电的影响

镁（镁2+)是多种细胞功能的必需矿物质。这种离子浓度低于生理浓度会导致海马切片和神经元培养物中的神经元反复放电。这些癫痫样放电最初对应用ñ-甲基-D-天冬氨酸 (NMDA) 受体拮抗剂，但这些拮抗剂可能会因长期暴露于低 [Mg2+]，当细胞外 Ca2+减少发生，典型的发作期，表明没有突触连接。本文提出的研究旨在研究减少 [Mg2+] 在非突触癫痫样活动 (NSEA) 的诱导过程中。作为实验方案，使用含有高 K 的浴液在大鼠海马齿状回 (DG) 中诱导 NSEA+和零添加钙2+. 此外，使用代表 DG 颗粒层组织的电化学特性的数学模型进行计算机模拟。实验结果表明，[Mg2+] 导致发作期持续时间延长和发作间期缩短，从而加剧癫痫样放电。计算机模拟表明 Mg 的减少2+水平通过减少表面电荷屏蔽和降低 Na/K 泵活性的共同作用来加强癫痫样放电。