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PMID: 9651206 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

The sodium channel Scn8a is the major contributor to the postnatal developmental increase of sodium current density in spinal motoneurons.

García KD, Sprunger LK, Meisler MH, Beam KG

Abstract

Sodium currents were recorded from motoneurons that were isolated from mice at postnatal days 0-8 (P0-P8) and maintained in culture for 12-24 hr. Motoneurons from normal mice exhibited a more than threefold increase in peak sodium current density from P0 to P8. For mice lacking a functional Scn8a sodium channel gene, motoneuronal sodium current density was comparable at P0 to that of normal mice but failed to increase from P0 to P8. The absence of Scn8a sodium channels is associated with the phenotype "motor end plate disease," which is characterized by a progressive neuromuscular failure and is fatal by 3-4 postnatal weeks. Thus, it appears that the development and function of mature motoneurons depends on the postnatal induction of Scn8a expression.

MeSH Terms
Animals Animals, Newborn Mice Mice, Inbred C3H Mice, Transgenic Motor Neurons/physiology RNA, Messenger/analysis Sodium Channels/physiology Spinal Cord/cytology,growth & development,physiology
Chemicals
RNA, Messenger Sodium Channels
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
García K D
Department of Anatomy and Neurobiology, Colorado State University, Fort Collins, Colorado 80523-1670, USA.
Sprunger L K
Meisler M H
Beam K G
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Article Info
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
Abbr.
J Neurosci
ISSN
0270-6474
Published
1998-07-15
Pages
5234-9
Language
English
Region
United States
NLM ID
8102140
PMCID
PMC6793491
Subset
IM
Grants
NHLBI NIH HHS · HL02972 · United States
NINDS NIH HHS · R01 NS024444 · United States
NINDS NIH HHS · R01 NS034509 · United States
NINDS NIH HHS · NS34509 · United States
NINDS NIH HHS · NS24444 · United States
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