Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1992-6-3
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-3623
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1147-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
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.
pubmed:affiliation
Institute of Endocrinology and Gerontology, Bulgarian Medical Academy, Sofia.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't