Embryonic neuroepithelial sodium transport, the resulting physiological potential, and cranial development

We have shown that the amiloride/novobiocin-sensitive sodium transport system of adult animal integuments is first observed in embryonic surface ectoderm and show here that this physiology is retained in this ectoderm following the closure of the neural folds. Unidirectional transport of Na+ out of the neural tube lumen results in a potential difference on the order of 40-90 mV, negative with respect to the abluminal surface. This transneural tube potential can be collapsed by iontophoresis of Na+ channel blockers amiloride or benzamil into the lumen, leading to severe cranial defects and incomplete morphogenesis. Modestly increasing the transneural tube potential with injection of novobiocin into the lumen also produces a lesser degree of developmental abnormality. We discuss the ways in which this physiology may help control the organization of the early nervous system.