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Distribution of the voltage‐gated sodium channel Na v 1.7 in the rat: Expression in the autonomic and endocrine systems
Author(s) -
Morinville Anne,
Fundin Bengt,
Meury Luc,
Juréus Anders,
Sandberg Kristian,
Krupp Johannes,
Ahmad Sultan,
O'Donnell Dajan
Publication year - 2007
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.21484
Subject(s) - biology , sodium channel , in situ hybridization , endocrinology , medicine , endocrine system , tetrodotoxin , homeostasis , neuroscience , ganglion , autonomic ganglion , autonomic nervous system , sodium , hormone , gene expression , heart rate , gene , chemistry , biochemistry , blood pressure , organic chemistry
It is generally accepted that the voltage‐gated, tetrodotoxin‐sensitive sodium channel, Na V 1.7, is selectively expressed in peripheral ganglia. However, global deletion in mice of Na V 1.7 leads to death shortly after birth (Nassar et al. [2004] Proc. Natl. Acad. Sci. U. S. A. 101:12706–12711), suggesting that this ion channel might be more widely expressed. To understand better the potential physiological function of this ion channel, we examined Na V 1.7 expression in the rat by in situ hybridization and immunohistochemistry. As expected, highest mRNA expression levels are found in peripheral ganglia, and the protein is expressed within these ganglion cells and on the projections of these neurons in the central nervous system. Importantly, we found that Na V 1.7 is present in discrete rat brain regions, and the unique distribution pattern implies a central involvement in endocrine and autonomic systems as well as analgesia. In addition, Na V 1.7 expression was detected in the pituitary and adrenal glands. These results indicate that Na V 1.7 is not only involved in the processing of sensory information but also participates in the regulation of autonomic and endocrine systems; more specifically, it could be implicated in such vital functions as fluid homeostasis and cardiovascular control. J. Comp. Neurol. 504:680–689, 2007. © 2007 Wiley‐Liss, Inc.

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