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首页> 外文期刊>The European Journal of Neuroscience >Cellular anatomy, physiology and epileptiform activity in the CA3 region of Dcx knockout mice: a neuronal lamination defect and its consequences.
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Cellular anatomy, physiology and epileptiform activity in the CA3 region of Dcx knockout mice: a neuronal lamination defect and its consequences.

机译：Dcx基因敲除小鼠CA3区的细胞解剖结构，生理学和癫痫样活动：神经元层压缺陷及其后果。

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摘要

We report data on the neuronal form, synaptic connectivity, neuronal excitability and epileptiform population activities generated by the hippocampus of animals with an inactivated doublecortin gene. The protein product of this gene affects neuronal migration during development. Human doublecortin (DCX) mutations are associated with lissencephaly, subcortical band heterotopia, and syndromes of intellectual disability and epilepsy. In Dcx(-/Y) mice, CA3 hippocampal pyramidal cells are abnormally laminated. The lamination defect was quantified by measuring the extent of the double, dispersed or single pyramidal cell layer in the CA3 region of Dcx(-/Y) mice. We investigated how this abnormal lamination affected two groups of synapses that normally innervate defined regions of the CA3 pyramidal cell membrane. Numbers of parvalbumin (PV)-containing interneurons, which contact peri-somatic sites, were not reduced in Dcx(-/Y) animals. Pyramidal cells in double, dispersed or single layers received PV-containing terminals. Excitatory mossy fibres which normally target proximal CA3 pyramidal cell apical dendrites apparently contact CA3 cells of both layers in Dcx(-/Y) animals but sometimes on basilar rather than apical dendrites. The dendritic form of pyramidal cells in Dcx(-/Y) animals was altered and pyramidal cells of both layers were more excitable than their counterparts in wild-type animals. Unitary inhibitory field events occurred at higher frequency in Dcx(-/Y) animals. These differences may contribute to a susceptibility to epileptiform activity: a modest increase in excitability induced both interictal and ictal-like discharges more effectively in tissue from Dcx(-/Y) mice than from wild-type animals.
机译：我们报告了由灭活的双皮质素基因的动物海马产生的神经元形式，突触连接性，神经元兴奋性和癫痫样种群活动的数据。该基因的蛋白质产物影响发育过程中的神经元迁移。人双皮质素（DCX）突变与小脑，皮层下带异位症和智力障碍和癫痫综合征相关。在Dcx（-/ Y）小鼠中，CA3海马锥体细胞被异常层压。通过测量Dcx（-/ Y）小鼠CA3区域中双，分散或单个锥体细胞层的程度来量化层压缺陷。我们研究了这种异常的叠层如何影响通常会支配CA3锥体细胞膜定义区域的两组突触。在Dcx（-/ Y）动物中，接触体周部位的含小白蛋白（PV）的中间神经元的数量没有减少。双层，分散或单层的金字塔形细胞接受含PV的末端。通常以近端CA3锥体细胞顶端树突为靶的兴奋性苔藓纤维显然会接触Dcx（-/ Y）动物中两层的CA3细胞，但有时会位于基底而不是顶端树突上。 Dcx（-/ Y）动物中的锥体细胞的树突形态发生了变化，并且两层锥体细胞都比野生型动物中的锥体细胞更易激发。在Dcx（-/ Y）动物中，单一的抑制性田间事件发生频率更高。这些差异可能导致对癫痫样活动的敏感性：兴奋性的适度增加在Dcx（-/ Y）小鼠的组织中比在野生型动物中更有效地诱导了发作间和发作样放电。

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