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Nav2/NaG Channel Is Involved in Control of Salt-Intake Behavior in the CNS
Open accessAbstract
Na v 2/NaG is a putative sodium channel, whose physiological role has long been an enigma. We generated Nav2 gene-deficient mice by inserting the lacZ gene. Analysis of the targeted mice allowed us to identify Na v 2-producing cells by examining the lacZ expression. Besides in the lung, heart, dorsal root ganglia, and Schwann cells in the peripheral nervous system,Na v 2 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 v 2-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 v 2 channel plays an important role in the central sensing of body-fluid sodium level and regulation of salt intake behavior.
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Gene-targeting studies of mammalian behavior: is it the mutation or the background genotype?
Gerlai, R. (1996) · Trends in Neurosciences · doi:10.1016/s0166-2236(96)20020-7 · Cited by 881
Cited by
Verkhratsky, A., & Nedergaard, M. (2018) · Physiological Reviews · doi:10.1152/physrev.00042.2016 · Cited by 1,678
Voltage‐gated sodium channels at 60: structure, function and pathophysiology
Catterall, W. A. (2012) · The Journal of Physiology · doi:10.1113/jphysiol.2011.224204 · Cited by 719
Voltage-gated sodium channels: structure, function, pharmacology, and clinical indications
de Lera Ruiz, M., & Kraus, R. L. (2015) · Journal of Medicinal Chemistry · doi:10.1021/jm501981g · Cited by 548
Transcriptional and epigenomic landscapes of CNS and non-CNS vascular endothelial cells
Sabbagh, M. F., Heng, J. S., Luo, C., Castanon, R. G., Nery, J. R., Rattner, A., Goff, L. A., Ecker, J. R., & Nathans, J. (2018) · eLife · doi:10.7554/elife.36187 · Cited by 245
McKinley, M. J., Yao, S. T., Uschakov, A., McAllen, R. M., Rundgren, M., & Martelli, D. (2015) · Acta Physiologica · doi:10.1111/apha.12487 · Cited by 180
Metadata
- Authors
- Watanabe, E., Fujikawa, A., Matsunaga, H., Yasoshima, Y., Sako, N., Yamamoto, T., Saegusa, C., & Noda, M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2000-10-15
- Volume
- 20
- Issue
- 20
- Pages
- 7743-7751
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1874317695
- Cited by
- 170
- References
- 1
- FWCI
- 1.46
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Watanabe, E., Fujikawa, A., Matsunaga, H., Yasoshima, Y., Sako, N., Yamamoto, T., Saegusa, C., & Noda, M. (2000). Nav2/NaG Channel Is Involved in Control of Salt-Intake Behavior in the CNS. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.20-20-07743.2000
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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