Neuronal Death and Perinatal Lethality in Voltage-Gated Sodium Channel αII-Deficient Mice
作者： R. Planells-Cases , M. Caprini , J. Zhang , E.M. Rockenstein , R.R. Rivera
DOI: 10.1016/S0006-3495(00)76829-9
关键词: Immunology 、 Cell biology 、 Neocortex 、 Apoptosis 、 Programmed cell death 、 Sodium channel 、 Knockout mouse 、 Brainstem 、 Biology 、 Hippocampus 、 Embryogenesis
摘要: Neural activity is crucial for cell survival and fine patterning of neuronal connectivity during neurodevelopment. To investigate the role in vivo sodium channels (NaCh) these processes, we generated knockout mice deficient brain NaChalpha(II). NaChalpha(II)(-/-) were morphologically organogenically indistinguishable from their NaChalpha(+/-) littermates. Notwithstanding, died perinatally with severe hypoxia massive apoptosis, notably brainstem. Sodium channel currents recorded cultured neurons sharply attenuated. Death appears to arise consequent brainstem deficiency NaChalpha(II) expression is, therefore, redundant embryonic development but essential postnatal survival.
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