Please use this identifier to cite or link to this item: http://hdl.handle.net/2067/1460
DC FieldValueLanguage
dc.contributor.authorCammalleri, Maurizio-
dc.contributor.authorCervia, Davide-
dc.contributor.authorDal Monte, Massimo-
dc.contributor.authorMartini, Davide-
dc.contributor.authorLangenegger, Daniel-
dc.contributor.authorFehlmann, Dominique-
dc.contributor.authorFeuerbach, Dominik-
dc.contributor.authorPavan, Barbara-
dc.contributor.authorHoyer, Daniel-
dc.contributor.authorBagnoli, Paola-
dc.date.accessioned2011-03-21T13:12:46Z-
dc.date.available2011-03-21T13:12:46Z-
dc.date.issued2006-
dc.identifier.citationCammalleri, M. et al. 2006. Compensatory changes in the hippocampus of somatostatin knockout mice: upregulation of somatostatin receptor 2 and its function in the control of bursting activity and synaptic transmission. "European Journal of Neuroscience" 23:2404-2422it
dc.identifier.issn0953-816X-
dc.identifier.urihttp://hdl.handle.net/2067/1460-
dc.descriptionL'articolo è disponibile sul sito dell'editore http://onlinelibrary.wiley.com/it
dc.description.abstractSomatostatin-14 (SRIF) colocalizes with GABA in the hippocampus and regulates neuronal excitability. A role of SRIF in the control of seizures has been proposed although its exact contribution requires some clarification. In particular, SRIF knock out (KO) mice do not exhibit spontaneous seizures, indicating that compensatory changes may occur in KO. In the KO hippocampus, we examined whether specific SRIF receptors and/or the cognate peptide cortistatin-14 (CST) compensate for SRIF’s absence. We found increased levels of both sst2 receptors (sst2) and CST and we explored the functional consequences of sst2 compensation on bursting activity and synaptic responses in hippocampal slices. Bursting was decreased by SRIF in wild type (WT) mice, but it was not affected by either CST or sst2 agonist and antagonist. sst4 agonist increased bursting frequency in either WT or KO. In WT, but not in KO, its effects were blocked by agonizing or antagonizing sst2, suggesting that sst2 and sst4 are functionally coupled in the WT hippocampus. Bursting was reduced in KO as compared to WT and was increased upon application of sst2 antagonist while SRIF, CST and sst2 agonist had no effect. At the synaptic level, we observed that in WT, SRIF decreased excitatory postsynaptic potentials which were, in contrast, increased by sst2 antagonist in KO. We conclude that sst2 compensates for SRIF absence and that its upregulation is responsible for reduced bursting and decreased excitatory transmission in KO mice. We suggest that a critical density of sst2 is needed to control hippocampal activity.it
dc.language.isoenit
dc.publisherWiley-Blackwellit
dc.subjectCortistatinit
dc.subjectHippocampal slicesit
dc.subjectSomatostatin analoguesit
dc.subjectTransgenic miceit
dc.titleCompensatory changes in the hippocampus of somatostatin knockout mice: upregulation of somatostatin receptor 2 and its function in the control of bursting activity and synaptic transmissionit
dc.typeArticleit
dc.identifier.doi10.1111/j.1460-9568.2006.04770.xit
item.fulltextWith Fulltext-
item.grantfulltextopen-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeArticle-
item.cerifentitytypePublications-
Appears in Collections:DISA - Archivio della produzione scientifica
Files in This Item:
File Description SizeFormat
Cammalleri et al-EJN 2006 1.pdf49.15 kBAdobe PDFView/Open
Show simple item record

Page view(s)

2
Last Week
0
Last month
1
checked on Dec 1, 2020

Download(s)

5
checked on Dec 1, 2020

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.