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首页> 外文期刊>The European Journal of Neuroscience >Dual effects of NMDA receptor activation on polysialylated neural cell adhesion molecule expression during brainstem postnatal development.
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Dual effects of NMDA receptor activation on polysialylated neural cell adhesion molecule expression during brainstem postnatal development.

机译:NMDA受体激活对脑干出生后发育过程中多唾液酸化神经细胞粘附分子表达的双重影响。

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摘要

Here we show a dual role of N-methyl-d-aspartate receptor (NMDAR) activation in controlling polysialylated neural cell adhesion molecule (PSA-NCAM) dynamic expression in the dorsal vagal complex (DVC), a gateway for many primary afferent fibres. In this structure the overall expression of PSA-NCAM decreases during the first 2 weeks after birth to persist only at synapses in the adult. Electrical stimulation of the vagal afferents causes a rapid increase of PSA-NCAM expression both in vivo and in acute slices before postnatal day (P) 14 whereas a similar stimulation induces a decrease after P15. Inhibition of NMDAR activity in vitro completely prevented these changes. These regulations depend on calmodulin activation and cGMP production at all stages. By contrast, blockade of neuronal nitric oxide synthase (nNOS) prevented these changes only after P10 in agreement with its late expression in the DVC. The pivotal role of NMDAR is also supported by the observation that chronic blockade induces a dramatic decrease in PSA-NCAM expression.
机译:在这里,我们显示了N-甲基-d-天冬氨酸受体(NMDAR)激活在控制背迷走神经复合体(DVC)(许多初级传入纤维的通道)中的多唾液酸化神经细胞粘附分子(PSA-NCAM)动态表达中的双重作用。在这种结构中,PSA-NCAM的总体表达在出生后的前两周下降,仅在成年人的突触中持续存在。迷走神经传入的电刺激会导致出生后一天(P)14之前的体内和急性切片中PSA-NCAM表达迅速增加,而类似的刺激会导致P15之后的PSA-NCAM表达降低。体外抑制NMDAR活性完全阻止了这些变化。这些法规取决于钙调蛋白激活和cGMP在所有阶段的生产。相比之下,对神经元一氧化氮合酶(nNOS)的阻止只能在P10后与其在DVC中的晚期表达相一致才能阻止这些变化。慢性阻塞引起PSA-NCAM表达急剧下降的观察也支持了NMDAR的关键作用。

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