Voltage-sensitive Na+ channels increase in number in newborn rat brain after in utero hypoxia.
The effect of chronic in utero hypoxia on voltage-sensitive Na+ channels in newborn rat brain was investigated by means of ligand binding and autoradiography with [3H]saxitoxin (STX, Na+ channel ligand). We found that: (a) binding properties were different between hypoxic and control brains with alinear Scatchard plots in hypoxic brain versus linear ones in the control; (b) STX binding density increased greatly in response to hypoxic stimulation; and (c) the hypoxia-induced increase in STX binding was heterogeneous in various brain areas. We conclude that chronic hypoxia in utero alters the expression of Na+ channels and induces an up-regulation of Na+ channel density as a function of brain area. This is the first report of this phenomenon and we believe that the increased Na+ channels may play an important role in the etiology of neurological disorders such as epilepsy.
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Department of Pediatrics (Section of Respiratory Medicine, Laboratory of Respiratory Neurobiology), Yale University School of Medicine, New Haven, CT 06510.
Haddad
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D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D002908:Chronic Disease; D005260:Female; D005311:Fetal Hypoxia / Q000378:metabolism*; D002534:Hypoxia, Brain / Q000378:metabolism*; D011247:Pregnancy; D011869:Radioligand Assay; D051381:Rats; D017207:Rats, Sprague-Dawley; D015222:Sodium Channels / Q000378:metabolism*
D015222:Sodium Channels