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rdf:type |
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lifeskim:mentions |
umls-concept:C0001443,
umls-concept:C0019564,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0030685,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0039062,
umls-concept:C0220839,
umls-concept:C0391871,
umls-concept:C0439799,
umls-concept:C0678226,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1963578
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pubmed:issue |
3
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pubmed:dateCreated |
2004-9-21
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pubmed:abstractText |
The voltage-gated Ca(2+) channels responsible for synaptic transmission at CA3-CA1 synapses are mainly P/Q- and N-types. It has been shown that tonic inhibition of transmission due to activation of adenosine A(1) receptors occurs at this synapse. We have recently developed a technique to monitor synaptically released glutamate which is based on synaptically induced glial depolarisation. Using this technique, we have examined the effects of different voltage-gated Ca(2+) channel blockers on glutamate release. Under conditions in which the adenosine A(1) receptor was not blocked, omega-AgaIVA (a P/Q-type voltage-gated Ca(2+) channel blocker) suppressed synaptically induced glial depolarisation to a greater extent than omega-CgTxGVIA (an N-type voltage-gated Ca(2+) channel blocker) did. In contrast, in the presence of an adenosine A(1) receptor antagonist, omega-AgaIVA was less effective at suppressing synaptically induced glial depolarisation than omega-CgTxGVIA. These results indicate that, in the absence of adenosine A(1) receptor-mediated tonic inhibition, the contribution of N-type is much greater than that of P-type, and that N-types are the primary target of tonic inhibition in normal conditions in which adenosine A(1) receptor-mediated tonic inhibition is present.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/8-cyclopentyl-1,3-dimethylxanthine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine A1 Receptor Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine A1 Receptor Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels, N-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/N(6)-cyclopentyladenosine,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Adenosine A1,
http://linkedlifedata.com/resource/pubmed/chemical/Theophylline,
http://linkedlifedata.com/resource/pubmed/chemical/omega-Agatoxin IVA,
http://linkedlifedata.com/resource/pubmed/chemical/omega-Conotoxin GVIA
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0014-2999
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
24
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pubmed:volume |
499
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
265-74
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:15381048-Adenosine,
pubmed-meshheading:15381048-Adenosine A1 Receptor Agonists,
pubmed-meshheading:15381048-Adenosine A1 Receptor Antagonists,
pubmed-meshheading:15381048-Animals,
pubmed-meshheading:15381048-Calcium Channel Blockers,
pubmed-meshheading:15381048-Calcium Channels, N-Type,
pubmed-meshheading:15381048-Dose-Response Relationship, Drug,
pubmed-meshheading:15381048-Glutamic Acid,
pubmed-meshheading:15381048-Hippocampus,
pubmed-meshheading:15381048-Male,
pubmed-meshheading:15381048-Rats,
pubmed-meshheading:15381048-Rats, Wistar,
pubmed-meshheading:15381048-Receptor, Adenosine A1,
pubmed-meshheading:15381048-Synapses,
pubmed-meshheading:15381048-Synaptic Transmission,
pubmed-meshheading:15381048-Theophylline,
pubmed-meshheading:15381048-omega-Agatoxin IVA,
pubmed-meshheading:15381048-omega-Conotoxin GVIA
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pubmed:year |
2004
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pubmed:articleTitle |
Adenosine A(1)-receptor-mediated tonic inhibition of glutamate release at rat hippocampal CA3-CA1 synapses is primarily due to inhibition of N-type Ca(2+) channels.
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pubmed:affiliation |
Laboratory of Cellular Neurobiology, School of Life Science, Tokyo University of Pharmacy and Life Science, Hachioji, Tokyo 192-0392, Japan.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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