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Medientyp:
E-Artikel
Titel:
A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons
Beteiligte:
Rush, Anthony M.;
Dib-Hajj, Sulayman D.;
Liu, Shujun;
Cummins, Theodore R.;
Black, Joel A.;
Waxman, Stephen G.
Erschienen:
Proceedings of the National Academy of Sciences, 2006
Erschienen in:Proceedings of the National Academy of Sciences
Sprache:
Englisch
DOI:
10.1073/pnas.0602813103
ISSN:
0027-8424;
1091-6490
Entstehung:
Anmerkungen:
Beschreibung:
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Disease-producing mutations of ion channels are usually characterized as producing hyperexcitability or hypoexcitability. We show here that a single mutation can produce hyperexcitability in one neuronal cell type and hypoexcitability in another neuronal cell type. We studied the functional effects of a mutation of sodium channel Na
<jats:sub>v</jats:sub>
1.7 associated with a neuropathic pain syndrome, erythermalgia, within sensory and sympathetic ganglion neurons, two cell types where Na
<jats:sub>v</jats:sub>
1.7 is normally expressed. Although this mutation depolarizes resting membrane potential in both types of neurons, it renders sensory neurons hyperexcitable and sympathetic neurons hypoexcitable. The selective presence, in sensory but not sympathetic neurons, of the Na
<jats:sub>v</jats:sub>
1.8 channel, which remains available for activation at depolarized membrane potentials, is a major determinant of these opposing effects. These results provide a molecular basis for the sympathetic dysfunction that has been observed in erythermalgia. Moreover, these findings show that a single ion channel mutation can produce opposing phenotypes (hyperexcitability or hypoexcitability) in the different cell types in which the channel is expressed.
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