Linked Life Data

15548214

Source:http://linkedlifedata.com/resource/pubmed/id/15548214

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2004-11-19
pubmed:abstractText
Somatostatin-14 [somatotropin release-inhibiting factor (SRIF)] reduces hippocampal epileptiform activity but the contribution of its specific receptors (sst1-5) is poorly understood. We have focused on the role of sst1 and sst2 in mediating SRIF modulation of epilepsy using hippocampal slices of wild-type (WT) and sst1 or sst2 knockout (KO) mice. Recordings of epileptiform discharge induced by Mg2+ -free medium with 4-aminopyridine were performed from the CA3 region before and after the application of SRIF compounds. In WT mice, SRIF and the sst1 agonist CH-275 reduce epilepsy whereas sst1 blockade with its antagonist SRA-880 increases the bursting discharge. Activation of sst2 does not affect the bursting frequency unless its agonist octreotide is applied with SRA-880, indicating that sst1 masks sst2-mediated modulation of epilepsy. In sst1 KO mice: (i) the bursting frequency is lower than in WT; (ii) SRIF, CH-275 and SRA-880 are ineffective on epilepsy and (iii) octreotide is also devoid of effects, whereas blockade of sst2 with the antagonist D-Tyr8 Cyn 154806 increases the bursting frequency. In sst2 KO mice, the SRIF ligand effects are similar to those in WT. In the whole hippocampus of sst1 KO mice, sst2 mRNA, protein and binding are higher than in WT and reverse transcription-polymerase chain reaction of the CA3 subarea confirms an increase of the sst2 messenger. We conclude that sst1 mediates inhibitory actions of SRIF and that interactions between sst1 and sst2 may prevent sst2 modulation of epilepsy. We suggest that, in sst1 KO mice, activation of over-expressed sst2 reduces the bursting frequency, indicating that sst2 density represents the rate-limiting factor for ss(2-mediated modulation of epilepsy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2711-21
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15548214-4-Aminopyridine, pubmed-meshheading:15548214-Action Potentials, pubmed-meshheading:15548214-Analysis of Variance, pubmed-meshheading:15548214-Animals, pubmed-meshheading:15548214-Binding Sites, pubmed-meshheading:15548214-Blotting, Western, pubmed-meshheading:15548214-Dose-Response Relationship, Drug, pubmed-meshheading:15548214-Epilepsy, pubmed-meshheading:15548214-Female, pubmed-meshheading:15548214-Gene Expression Regulation, pubmed-meshheading:15548214-Hippocampus, pubmed-meshheading:15548214-Male, pubmed-meshheading:15548214-Mice, pubmed-meshheading:15548214-Mice, Inbred C57BL, pubmed-meshheading:15548214-Mice, Knockout, pubmed-meshheading:15548214-Neurons, pubmed-meshheading:15548214-Potassium Channel Blockers, pubmed-meshheading:15548214-RNA, Messenger, pubmed-meshheading:15548214-Radioligand Assay, pubmed-meshheading:15548214-Receptors, Somatostatin, pubmed-meshheading:15548214-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15548214-Somatostatin
pubmed:year
2004
pubmed:articleTitle
Somatostatin receptors differentially affect spontaneous epileptiform activity in mouse hippocampal slices.
pubmed:affiliation
Dipartimento di Fisiologia e Biochimica 'G. Moruzzi', Università di Pisa, 56127 Pisa, Italy.
pubmed:publicationType
Journal Article, Comparative Study, In Vitro, Research Support, Non-U.S. Gov't