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首页> 外文期刊>The European Journal of Neuroscience >Irreversible loss of a subpopulation of cortical interneurons in the absence of glutamatergic network activity.
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Irreversible loss of a subpopulation of cortical interneurons in the absence of glutamatergic network activity.

机译：在没有谷氨酸能网络活性的情况下，皮质中神经元亚群的不可逆丢失。

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Abstract In the cerebral cortex of mammals, gamma-aminobutyric acid (GABA)ergic neurons represent 15-25% of all neurons, depending on the species and area being examined. Because converging evidence suggests that activity may play an important role in the neuritic maturation and synaptic function of GABAergic neurons, it is feasible that activity plays a role in the regulation of the proportion of GABAergic neurons. Here we provide direct evidence that early in cortical development activity blockade may deplete the network of a subpopulation of GABA immunoreactive neurons characterized by their small size and late generation in vitro. In a period of time coinciding with the emergence of synchronous network activity, the survival and morphological differentiation of GABAergic neurons was influenced by long-term blockade of synaptic activity. While GABA(A) receptor antagonists had a minor promoting effect on interneuronal survival during the second week in vitro, antagonists of ionotropic glutamate receptors strongly impaired survival and differentiation of immature GABAergic interneurons. Interneuronal loss was more severe when N-methyl-d-aspartate receptors were blocked than after blockade of alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA)/kainate receptors. The decrease in the density of GABAergic neurons was irreversible, but could be prevented by the simultaneous addition of brain-derived neurotrophic factor (BDNF). These results suggest that there is a narrow time window during neocortical development when glutamatergic activity, and specially NMDA receptor stimulation, is crucial to assure survival and maturation of a subpopulation of late developing GABAergic interneurons.
机译：摘要在哺乳动物的大脑皮层中，γ-氨基丁酸（GABA）能神经元占所有神经元的15-25％，具体取决于所检查的物种和区域。由于越来越多的证据表明，活性可能在GABA能神经元的神经成熟和突触功能中起重要作用，因此可行的是，活性在GABA能神经元的比例调节中起作用。在这里，我们提供了直接的证据，即早期皮质发育活动受阻可能耗尽了GABA免疫反应性神经元亚群的网络，这些神经元的特征是其体积小且在体外较晚。在一段时间内与同步网络活动的出现相吻合，GABA能神经元的存活和形态分化受到突触活动的长期阻断的影响。尽管GABA（A）受体拮抗剂在体外第二周内对神经元间的存活有较小的促进作用，但离子型谷氨酸受体的拮抗剂却强烈损害了未成熟GABA能性神经元的存活和分化。 N-甲基-d-天冬氨酸受体被阻断时，神经元间丢失比α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）/海藻酸酯受体被阻断后更为严重。 GABA能神经元密度的降低是不可逆的，但可以通过同时添加脑源性神经营养因子（BDNF）来防止。这些结果表明，当谷氨酸能活性，特别是NMDA受体刺激，对于确保晚期发育的GABA能中间神经元的亚群的存活和成熟至关重要时，在新皮质发育过程中存在狭窄的时间窗。

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