Voltage-sensitive Na+ channels increase in number in newborn rat brain after in utero hypoxia.

Abstract

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.

• Authors: Y Xia, G G Haddad
• Journal: Brain research (Brain Res) Vol. 635 Issue 1-2 Pg. 339-44 (Jan 28 1994) ISSN: 0006-8993 [Print] Netherlands
• PMID: 8173974 (Publication Type: Journal Article)

Chemical References

• Sodium Channels

Topics

• Animals
• Animals, Newborn (metabolism)
• Chronic Disease
• Female
• Fetal Hypoxia (metabolism)
• Hypoxia, Brain (metabolism)
• Pregnancy
• Radioligand Assay
• Rats
• Rats, Sprague-Dawley
• Sodium Channels (metabolism)