Nav2/NaG Channel Is Involved in Control of Salt-Intake Behavior in the CNS

Open Access
Publisher Website
Google Scholar
Abstract
Nav2/NaG is a putative sodium channel, whose physiological role has long been an enigma. We generatedNav2 gene-deficient mice by inserting the lacZ gene. Analysis of the targeted mice allowed us to identify Nav2-producing cells by examining the lacZ expression. Besides in the lung, heart, dorsal root ganglia, and Schwann cells in the peripheral nervous system, Nav2 was expressed in neurons and ependymal cells in restricted areas of the CNS, particularly in the circumventricular organs, which are involved in body-fluid homeostasis. Under water-depleted conditions,c-fos expression was markedly elevated in neurons in the subfornical organ and organum vasculosum laminae terminalis compared with wild-type animals, suggesting a hyperactive state in theNav2-null mice. Moreover, the null mutants showed abnormal intakes of hypertonic saline under both water- and salt-depleted conditions. These findings suggest that the Nav2 channel plays an important role in the central sensing of body-fluid sodium level and regulation of salt intake behavior.