Please use this identifier to cite or link to this item: http://hdl.handle.net/2067/1470
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dc.contributor.authorCervia, Davide-
dc.contributor.authorMartini, Davide-
dc.contributor.authorRistori, Chiara-
dc.contributor.authorCatalani, Elisabetta-
dc.contributor.authorTimperio, Anna Maria-
dc.contributor.authorBagnoli, Paola-
dc.contributor.authorCasini, Giovanni-
dc.date.accessioned2011-03-21T13:41:13Z-
dc.date.available2011-03-21T13:41:13Z-
dc.date.issued2008-
dc.identifier.citationCervia, D. et al. 2008. Modulation of the neuronal response to ischemia by somatostatin analogues in wild-type and knock-out mouse retinas. "Journal of Neurochemistry" 106(5): 2224-2235it
dc.identifier.issn0022-3042-
dc.identifier.urihttp://hdl.handle.net/2067/1470-
dc.descriptionL'articolo è disponibile sul sito dell'editore http://onlinelibrary.wiley.com/it
dc.description.abstractSomatostatin acts at five G protein-coupled receptors, sst1-sst5. In mouse ischemic retinas, the over-expression of sst2 (as in sst1 knock-out mice) results in reduction of cell death and glutamate release. Here, we reported that, in wild-type retinas, somatostatin, the multireceptor ligand pasireotide and the sst2 agonist octreotide decreased ischemia-induced cell death and that octreotide also decreased glutamate release. In contrast, cell death was increased by blocking sst2 with cyanamide. In sst2 over-expressing ischemic retinas, somatostatin analogues increased cell death, and octreotide also increased glutamate release. To explain this reversal of the anti-ischemic effect of somatostatin agonists in the presence of sst2 over-expression, we tested sst2 desensitisation due to internalisation or altered receptor function. We observed that: i) sst2 was not internalised, ii) among G protein-coupled receptor kinases (GRKs) and regulators of G protein signalling (RGSs), GRK1 and RGS1 expression increased following ischemia, iii) both GRK1 and RGS1 were down-regulated by octreotide in wild-type ischemic retinas, iv) octreotide down-regulated GRK1 but not RGS1 in sst2 over-expressing ischemic retinas. These results demonstrate that sst2 activation protects against retinal ischemia. However, in the presence of sst2 over-expression sst2 is functionally desensitised by agonists, possibly due to sustained RGS1 levels.it
dc.language.isoenit
dc.publisherWiley-Blackwellit
dc.subjectCell deathit
dc.subjectG protein-coupled receptor kinasesit
dc.subjectGlutamate releaseit
dc.subjectRegulators of G protein signallingit
dc.subjectSomatostatin receptorsit
dc.titleModulation of the neuronal response to ischemia by somatostatin analogues in wild-type and knock-out mouse retinasit
dc.typeArticleit
dc.identifier.doi10.1111/j.1471-4159.2008.05556.xit
item.fulltextWith Fulltext-
item.openairetypeArticle-
item.cerifentitytypePublications-
item.grantfulltextopen-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
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