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Title: | Modulation of the neuronal response to ischemia by somatostatin analogues in wild-type and knock-out mouse retinas | Authors: | Cervia, Davide Martini, Davide Ristori, Chiara Catalani, Elisabetta Timperio, Anna Maria Bagnoli, Paola Casini, Giovanni |
Keywords: | Cell death;G protein-coupled receptor kinases;Glutamate release;Regulators of G protein signalling;Somatostatin receptors | Issue Date: | 2008 | Publisher: | Wiley-Blackwell | Source: | Cervia, 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): 2224-2235 | Abstract: | Somatostatin 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. |
Description: | L'articolo è disponibile sul sito dell'editore http://onlinelibrary.wiley.com/ |
URI: | http://hdl.handle.net/2067/1470 | ISSN: | 0022-3042 | DOI: | 10.1111/j.1471-4159.2008.05556.x |
Appears in Collections: | DISA - Archivio della produzione scientifica |
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Cervia et al J Neurochem 2008 1.pdf | 139.86 kB | Adobe PDF | View/Open |
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