|
|
|
| Untersuchte Arbeit: Seite: 24, Zeilen: 24-32 |
Quelle: Stumm et al 2004 Seite(n): 11404, 11413, Zeilen: 11404:left col. 8-11 - right col. 1-5; 11413:right col. 36-42 |
|---|---|
| In non-neuronal cells, somatostatin has been shown to enhance death ligand- and mitochondria-mediated apoptosis (Guillermet et al., 2003), indicating that conserved signaling pathways in programmed cell death can be influenced by somatostatin receptors. Intracerebral applications of SSTR ligands before middle cerebral artery occlusion affect the infarct volume in a dose-dependent manner (Rauca et al., 1999), suggesting that somatostatin may influence neurodegeneration after brain ischemia. Activation and upregulation of somatostatin receptors type 2 in perifocal pyramidal neurons after focal ischemia were reported. Upregulation of these receptors is most likely the result of both somatostatin-derived and heterologous signals and may counteract somatostatin desensitization. Excessive activation of somatostatin receptors type 2 [in perifocal neurons by endogenous ligands is likely to account for the larger infarcts in wild-type mice than in somatostatin receptors type 2 -deficient mice (Stumm et al., 2004).] | [Page 11404]
Introduction [...] In non-neuronal cells, SSTR2 has been shown to enhance death ligand- and mitochondria-mediated apoptosis (Guillermet et al., 2003), indicating that conserved signaling pathways in programmed cell death can be influenced by SSTRs. Intracerebral applications of SSTR ligands before middle cerebral artery occlusion (MCAO) affect the infarct volume in a dose-dependent manner (Rauca et al., 1999), suggesting that SSTRs may influence neurodegeneration after brain ischemia. [Page 11413] Conclusion Together, this study provides the first evidence for activation and upregulation of SSTR2 in perifocal pyramidal neurons after focal ischemia. Upregulation of SSTR2 is most likely the result of both SSTR2-derived and heterologous signals and may counteract SSTR2 desensitization. Excessive activation of SSTR2 in perifocal neurons by endogenous ligands is likely to account for the larger infarcts in wild-type mice than in SSTR2-deficient mice. |
The source is mentioned in the end as one of several sources mentioned in this passage. This does not make clear that the whole passage is taken from the source and that some quotations are literal. |
|