Linked Life Data

17401576

Source:http://linkedlifedata.com/resource/pubmed/id/17401576

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-5-11
pubmed:abstractText
Voltage-gated K(+) channels are crucial for intrinsic neuronal plasticity and present a target for modulations by protein-protein interactions, notably, by exocytotic proteins demonstrated by us in several systems. Here, we investigated the interaction of a single Kv1.1 channel with syntaxin 1A. Syntaxin decreased the unitary conductance of all conductance states (two subconductances and a full conductance) and decreased their open probabilities by prolongation of mean closed dwell-times at depolarized potentials. However, at subthreshold potentials syntaxin 1A increased the probabilities of the subconductance states. Consequently, the macroscopic conductance is decreased at potentials above threshold and increased at threshold potentials. Numerical modeling based on steady-state and kinetic analyses suggests: (1) a mechanism whereby syntaxin controls activation gating by forcing the conductance pathway only via a sequence of discrete steps through the subconductance states, possibly via a breakdown of cooperative movements of voltage sensors that exist in Kv1.1; (2) a physiological effect, apparently paradoxical for an agent that reduces K(+) current, of attenuating neuronal firing frequency via an increase in K(+) shunting conductance. Such modulation of the gain of neuronal output in response to different levels of syntaxin is in accord with the suggested role for Kv1.1 in axonal excitability and synaptic efficacy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
454
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
477-94
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Interaction of syntaxin with a single Kv1.1 channel: a possible mechanism for modulating neuronal excitability.
pubmed:affiliation
Department of Physiology and Pharmacology, Sackler School of Medicine, Tel-Aviv University, 69978, Ramat-Aviv, Israel.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't