Source:http://linkedlifedata.com/resource/pubmed/id/11948007
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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001041,
umls-concept:C0006949,
umls-concept:C0016733,
umls-concept:C0030685,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0078844,
umls-concept:C0391871,
umls-concept:C0439799,
umls-concept:C0596235,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1704675,
umls-concept:C1963578
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pubmed:issue |
1
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pubmed:dateCreated |
2002-4-11
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pubmed:abstractText |
To clarify the mechanisms of action of antiepileptic drugs (AEDs), carbamazepine (CBZ) and zonisamide (ZNS), on exocytosis mechanisms, the present study determined the concentration-dependent action of CBZ and ZNS, as well as the interaction between these AEDs and voltage-sensitive Ca(2+) channel (VSCC) activity on basal, Ca(2+)- and K(+)-evoked acetylcholine (ACh) release in frontal cortex of freely moving rat using in vivo microdialysis. Perfusion with therapeutic-relevant concentrations of CBZ and ZNS increased basal ACh release, which was regulated by N-type VSCC predominantly and P-type VSCC weakly, whereas supratherapeutic-relevant concentrations of these AEDs reduced this release. The 3.4 mM Ca(2+)-evoked release, which was regulated by N-type VSCC selectively, but not by P-type VSCC, was increased by therapeutic-relevant concentrations of CBZ and ZNS, whereas this release was reduced by supratherapeutic-relevant concentrations of them. The 50 mM K(+)-evoked release, which was regulated by P-type VSCC predominantly and N-type VSCC weakly, was decreased by CBZ and ZNS, in a concentration-dependent manner. These findings indicate that the interplay between enhancement of basal ACh release and reduction of depolarization-related ACh release in the frontal cortex are at least partially involved in a common mechanism of antiepileptic action between CBZ and ZNS.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Carbamazepine,
http://linkedlifedata.com/resource/pubmed/chemical/Isoxazoles,
http://linkedlifedata.com/resource/pubmed/chemical/zonisamide
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0920-1211
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
49
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
49-60
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11948007-Acetylcholine,
pubmed-meshheading:11948007-Animals,
pubmed-meshheading:11948007-Calcium Channels,
pubmed-meshheading:11948007-Carbamazepine,
pubmed-meshheading:11948007-Diffusion,
pubmed-meshheading:11948007-Dose-Response Relationship, Drug,
pubmed-meshheading:11948007-Drug Interactions,
pubmed-meshheading:11948007-Frontal Lobe,
pubmed-meshheading:11948007-Isoxazoles,
pubmed-meshheading:11948007-Male,
pubmed-meshheading:11948007-Microdialysis,
pubmed-meshheading:11948007-Rats,
pubmed-meshheading:11948007-Rats, Wistar
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pubmed:year |
2002
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pubmed:articleTitle |
Interaction between carbamazepine, zonisamide and voltage-sensitive Ca2+ channel on acetylcholine release in rat frontal cortex.
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pubmed:affiliation |
Department of Neuropsychiatry, School of Medicine, University of Hirosaki, 036-8562, Hirosaki, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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