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癫痫低钙模型中海马对非突触性癫痫样同步化倾向的调节

Modulation of the hippocampal propensity to non- synaptic epileptiform synchronization in low-calcium model of epilepsy.

作者信息

Zapukhliak O S, Netsyk O V, Rasulova O S, Isaev D S

出版信息

Fiziol Zh (1994). 2016;62(6):19-24.

PMID:29762967
Abstract

The CA3 and CAI regions are the main stages of the "three-synaptic pathway", which plays a role in the generation of hyper-synchronous events in the hippocampus. Under certain experimental conditions, this brain structure might support pathological epileptiform synchronization that is independent of active chemical synaptic transmission. In present work, we estimated the conditions that would facilitate non- synaptic synchronization of the hippocampus. Non-synaptic epileptiform activity was induced in hippocampal slices by the omission calcium ions from the extracellular milieu. The propensity of hippocampal regions to nonsynaptic interactions was estimated by measuring the delay time neededfor the development of low-Ca²⁺ discharges in the CA3 and CAI. Next, an increase of neuronal excitability was induced by the pre- incubation ofhippocampal slices in 4-aminopyridine (4-AP) and by the reduction ofextracellular osmolarity. Pre-incubation of hippbcampal slices with 4-AP under normal osmotic conditions resulted in decreased latency for non-synaptic discharges in the CA3, but not in the CAl. However hypo-osmotic conditions caused increased excitability of the CA3 region, which resulted in decreased delay time for nonsynaptic discharges and this level of cellular excitability was not further enhanced by the pre-incubation with 4-AR.

摘要

CA3区和CA1区是“三突触通路”的主要阶段,该通路在海马体中高同步事件的产生中发挥作用。在某些实验条件下,这种脑结构可能支持独立于活跃化学突触传递的病理性癫痫样同步。在本研究中,我们评估了促进海马体非突触同步的条件。通过从细胞外环境中去除钙离子,在海马体切片中诱导出非突触性癫痫样活动。通过测量CA3区和CA1区低钙放电发展所需的延迟时间,评估海马体区域进行非突触相互作用的倾向。接下来,通过将海马体切片在4-氨基吡啶(4-AP)中预孵育以及降低细胞外渗透压来诱导神经元兴奋性增加。在正常渗透压条件下,用4-AP对海马体切片进行预孵育会导致CA3区非突触放电的潜伏期缩短,但CA1区没有这种现象。然而,低渗条件会导致CA3区兴奋性增加,这使得非突触放电的延迟时间缩短,并且这种细胞兴奋性水平不会因用4-AP预孵育而进一步增强。

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