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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0006772,
umls-concept:C0007776,
umls-concept:C0016295,
umls-concept:C0019564,
umls-concept:C0023977,
umls-concept:C0028066,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0040979,
umls-concept:C0042523,
umls-concept:C0231491,
umls-concept:C0243076,
umls-concept:C0441655,
umls-concept:C0547047,
umls-concept:C0753726
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pubmed:issue |
6
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pubmed:dateCreated |
1992-6-3
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pubmed:abstractText |
1. The binding activity of 5-HT1 receptors was studied in membrane fractions from the cerebral cortex and hippocampus of male Wistar rats treated orally for 13 days with the Ca(2+)-antagonists nifedipine (20 mg/kg), verapamil (50 mg/kg) and flunarizine (10 mg/kg) and with the calmodulin antagonist trifluoperazine (3 mg/kg). 2. The binding capacity and affinity of the 5-HT1 receptors in the cerebral cortex were significantly decreased after the treatment with the Ca(2+)-antagonists nifedipine, verapamil and flunarizine. The dissociation constant (Kd) was increased after the treatment with the calmodulin antagonist trifluoperazine. 3. In the hippocampus the 5-HT1 receptor affinity and number of binding sites were significantly reduced after the treatment with all four antagonists tested--nifedipine, verapamil, flunarizine and trifluoperazine, the Kd value being increased insignificantly after the flunarizine treatment. 4. The results obtained afford the suggestion that the reduction of 5-HT1 receptor activity is at least one of the results of the well known Ca(2+)-ions mediated automodulation of 5-HT release. The data confirm the view about the great importance of Ca(2+)-ions for the regulation of membrane neurotransmitter receptor activities.
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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/Calcium Channel Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Calmodulin,
http://linkedlifedata.com/resource/pubmed/chemical/Flunarizine,
http://linkedlifedata.com/resource/pubmed/chemical/Nifedipine,
http://linkedlifedata.com/resource/pubmed/chemical/Serotonin Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Trifluoperazine,
http://linkedlifedata.com/resource/pubmed/chemical/Verapamil
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pubmed:status |
MEDLINE
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pubmed:issn |
0306-3623
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
22
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1147-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1810811-Animals,
pubmed-meshheading:1810811-Calcium Channel Blockers,
pubmed-meshheading:1810811-Calmodulin,
pubmed-meshheading:1810811-Cerebral Cortex,
pubmed-meshheading:1810811-Flunarizine,
pubmed-meshheading:1810811-Hippocampus,
pubmed-meshheading:1810811-Kinetics,
pubmed-meshheading:1810811-Male,
pubmed-meshheading:1810811-Nifedipine,
pubmed-meshheading:1810811-Rats,
pubmed-meshheading:1810811-Rats, Inbred Strains,
pubmed-meshheading:1810811-Serotonin Antagonists,
pubmed-meshheading:1810811-Trifluoperazine,
pubmed-meshheading:1810811-Verapamil
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pubmed:year |
1991
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pubmed:articleTitle |
The long-term treatment with the Ca(2+)-antagonists nifedipine, verapamil, flunarizine and with the calmodulin antagonist trifluoperazine decreases the activity of 5-HT1 receptors in rat cerebral cortex and hippocampus.
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pubmed:affiliation |
Institute of Endocrinology and Gerontology, Bulgarian Medical Academy, Sofia.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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