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首页> 外文期刊>The European Journal of Neuroscience >Differential down-regulation of voltage-gated calcium channel currents by glutamate and BDNF in embryonic cortical neurons.
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Differential down-regulation of voltage-gated calcium channel currents by glutamate and BDNF in embryonic cortical neurons.

机译：谷氨酸和BDNF在胚胎皮质神经元中对电压门控钙通道电流的差异性下调。

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In the embryonic brain, post-mitotic cortical neurons migrate from their place of origin to their final location. Various external factors such as hormones, neurotransmitters or peptides regulate their migration. To date, however, only a few studies have investigated the effects of these external factors on the electrical properties of the newly formed embryonic cortical neurons. The aim of the present study was to determine whether glutamate and brain-derived neurotrophic factor (BDNF), known to regulate neuronal cell migration, could modulate currents through voltage-gated calcium channels (I(Ca)) in cortical neurons isolated from embryonic day 13 (E13) mouse foetuses. Whole cell recordings of I(Ca) showed that E13 cortical cells kept 1 day in vitro expressed functional low- and high-voltage activated (LVA and HVA) Ca(2+) channels of T-, L- and N-types. A 1-day glutamate treatment non-specifically inhibited LVA and HVA I(Ca) whereas BDNF down-regulated HVA with N-type I(Ca) being more depressed than L-type I(Ca). The glutamate-induced I(Ca) inhibition was mimicked by NMDA. BDNF exerted its action by recruiting trkB receptors and SKF-96365-sensitive channels. BAPTA prevented the glutamate- and the BDNF-dependent inhibition of I(ca), indicating a Ca(2+)-dependent mechanism of action. It is proposed that an influx of Ca(2+) through NMDA receptors depresses the expression of LVA and HVA Ca(2+) channels whereas a Ca(2+) influx through SKF-96365-sensitive TRPC (transient receptor potential protein of C subtype) channels preferentially inhibits the expression of HVA Ca(2+) channels. Glutamate and BDNF appear as potent modulators of the electrical properties of early post-mitotic neurons. By down-regulating I(Ca) they could exert a neuroprotective action on embryonic cortical neurons.
机译：在胚胎脑中，有丝分裂后的皮质神经元从其起源位置迁移到最终位置。各种外部因素，例如激素，神经递质或肽调节其迁移。然而，迄今为止，只有很少的研究调查了这些外部因素对新形成的胚胎皮质神经元电学性质的影响。本研究的目的是确定已知调节神经元细胞迁移的谷氨酸和脑源性神经营养因子（BDNF）是否可以通过电压门控钙通道（I（Ca））调节从胚胎日分离的皮层神经元的电流。 13（E13）小鼠胎儿。 I（Ca）的全细胞记录显示，体外维持1天的E13皮质细胞表达T型，L型和N型的功能性低压和高压激活（LVA和HVA）Ca（2+）通道。 1天的谷氨酸盐处理非特异性抑制LVA和HVA I（Ca），而BDNF下调HVA，N型I（Ca）比L型I（Ca）更为抑郁。 NMDA模拟谷氨酸诱导的I（Ca）抑制。 BDNF通过募集trkB受体和SKF-96365敏感通道发挥作用。 BAPTA阻止了谷氨酸和BDNF依赖的I（ca）抑制，表明Ca（2+）依赖的作用机制。有人提出，通过NMDA受体流入Ca（2+）会抑制LVA和HVA Ca（2+）通道的表达，而通过SKF-96365敏感的TRPC（C的瞬时受体电位蛋白）会流入Ca（2+）亚型）通道优先抑制HVA Ca（2+）通道的表达。谷氨酸和BDNF似乎是早期有丝分裂后神经元电学性质的有效调节剂。通过下调I（Ca），它们可以对胚胎皮质神经元发挥神经保护作用。

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