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Biophys J, June 2000, p. 2878-2891, Vol. 78, No. 6

Neuronal Death and Perinatal Lethality in Voltage-Gated Sodium Channel alpha II-Deficient Mice

R. Planells-Cases,* M. Caprini,* J. Zhang,* E. M. Rockenstein,dagger R. R. Rivera,* C. Murre,* E. Masliah,dagger and M. Montal*

Departments of  *Biology and  dagger Neurosciences, University of California San Diego, La Jolla, California

Neural activity is crucial for cell survival and fine patterning of neuronal connectivity during neurodevelopment. To investigate the role in vivo of sodium channels (NaCh) in these processes, we generated knockout mice deficient in brain NaChalpha II. NaChalpha II-/- mice were morphologically and organogenically indistinguishable from their NaChalpha +/- littermates. Notwithstanding, NaChalpha II-/- mice died perinatally with severe hypoxia and massive neuronal apoptosis, notably in the brainstem. Sodium channel currents recorded from cultured neurons of NaChalpha II-/- mice were sharply attenuated. Death appears to arise from severe hypoxia consequent to the brainstem deficiency of NaChalpha II. NaChalpha II expression is, therefore, redundant for embryonic development but essential for postnatal survival.

Biophys J, June 2000, p. 2878-2891, Vol. 78, No. 6
© 2000 by the Biophysical Society   0006-3495/00/06/2878/14  $2.00


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