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Reduced expression of voltage‐gated sodium channels in neurons cultured from trisomy 16 mouse hippocampus
Author(s) -
Stoll James,
Galdzicki Zygmunt
Publication year - 1996
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/s0736-5748(96)00051-2
Subject(s) - sodium channel , depolarization , hippocampal formation , hippocampus , tetrodotoxin , biology , conductance , neuroscience , microbiology and biotechnology , chemistry , sodium , biophysics , physics , organic chemistry , condensed matter physics
Voltage‐gated sodium channels are responsible for the initial depolarizing phase of the action potential. In hippocampal neurons cultured from trisomy 16 (Ts16) mice (a model for Down's syndrome), the maximum inward conductance mediated by these channels was reduced 47% relative to control diploid neurons. This reduced conductance was reflected in a 35% decrease in binding of radiolabeled saxitoxin, a sodium channel‐specific ligand, indicating expression of fewer channels in these neurons. The mRNAs encoding the α and β 1 subunits were, however, present at the same levels in Ts16 neurons and control diploid neurons. Thus, the altered regulation of voltage‐gated sodium channels in Ts16 neurons is apparently a post‐transcriptional event and possible mechanisms are discussed.