Linked Life Data

17031067

Source:http://linkedlifedata.com/resource/pubmed/id/17031067

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-10-19
pubmed:abstractText
Previous reports revealed up-regulation of L-type high voltage-gated calcium channels (HVCCs) in mouse brains with ethanol physical dependence. We investigated mechanisms of enhancement of L-type HVCC function using mouse cerebrocortical neurons exposed to 50 mM ethanol for 3 days and the brains of mouse physically dependent on ethanol. Ethanol facilitated 30 mM KCl-stimulated (45)Ca(2+) influx in dose- and duration-dependent manners, which was abolished by nifedipine, an inhibitor specific to L-type HVCCs, but not by inhibitors for other types of HVCCs. Increase in [(3)H]PN200-110 binding to the particulate fractions from the ethanol-treated neurons was due to increased B(max) value with no changes in K(d) value. Western blot analysis showed the increased expression of alpha1C, alpha1D, and alpha2/delta1 subunits with decreased beta4 subunit expression and no changes in expressions of alpha1A, alpha1B, alpha1F, and alpha2 subunits. A similar pattern of the changes in the expression of these subunits of L-type HVCCs were observed in the cerebral cortex from mouse with ethanol physical dependence. These results indicate that sustained ethanol exposure to the neurons induces up-regulation of L-type HVCCs, which is due to increased expressions of alpha1C, alpha1D, and alpha2/delta1 subunits, and produces no alterations in P/Q- and N-type HVCC functions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1347-8613
pubmed:author
pubmed:issnType
Print
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
221-30
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Increase in expression of alpha1 and alpha2/delta1 subunits of L-type high voltage-gated calcium channels after sustained ethanol exposure in cerebral cortical neurons.
pubmed:affiliation
Department of Pharmacology, Kawasaki Medical University, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't