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The Journal of Neuroscience, October 15, 2000, 20(20):7743-7751

Na_v2/NaG Channel Is Involved in Control of Salt-Intake Behavior in the CNS

Eiji Watanabe^{1, 2, 3}, Akihiro Fujikawa¹, Haruyuki Matsunaga¹, Yasunobu Yasoshima⁴, Noritaka Sako⁴, Takashi Yamamoto⁴, Chika Saegusa^{1, 3}, and Masaharu Noda^{1, 2, 3}

¹ Division of Molecular Neurobiology, and ² Center for Transgenic Animals and Plants, National Institute for Basic Biology, Myodaiji-cho, Okazaki 444-8585, ³ Department of Molecular Biomechanics, The Graduate University for Advanced Studies, Myodaiji-cho, Okazaki 444-8585, Japan, and ⁴ Department of Behavioral Physiology, Faculty of Human Sciences, Osaka University, 1-2 Yamadaoka, Suita 565-0871, Japan

Na_v2/NaG is a putative sodium channel, whose physiological role has long been an enigma. We generated Na_v2 gene-deficient mice by inserting the lacZ gene. Analysis of the targeted mice allowed us to identify Na_v2-producing cells by examining the lacZ expression. Besides in the lung, heart, dorsal root ganglia, and Schwann cells in the peripheral nervous system, Na_v2 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 the Na_v2-null mice. Moreover, the null mutants showed abnormal intakes of hypertonic saline under both water- and salt-depleted conditions. These findings suggest that the Na_v2 channel plays an important role in the central sensing of body-fluid sodium level and regulation of salt intake behavior.

Key words: sodium channel; knock-out mouse; circumventricular organs; salt appetite; body-fluid homeostasis; osmoreceptor

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Copyright © 2000 Society for Neuroscience  0270-6474/00/20207743-09$05.00/0

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