Changes in galanin and GalR1 gene expression in discrete brain regions after transient occlusion of the middle cerebral artery in female rats
2012 (English)In: Neuropeptides, ISSN 0143-4179, E-ISSN 1532-2785, Vol. 46, no 1, 19-27 p.Article in journal (Refereed) Published
Injury to neurons results in upregulation of galanin in some central and peripheral systems, and it has been suggested that this neuropeptide may play a protective and trophic role, primarily mediated by galanin receptor 2 (GalR2). The objective of the present study was to investigate galanin, GalR1, GalR2 and GalR3 gene expression in the female rat brain seven days after a 60-min unilateral occlusion of the middle cerebral artery followed by reperfusion. Quantitative real-time PCR was employed in punch-biopsies from the locus coeruleus, somatosensory cortex and dorsal hippocampal formation including sham-operated rats as controls. Galanin gene expression showed a ~2.5-fold increase and GalR1 a ~1.5-fold increase in the locus coeruleus of the ischemic hemisphere compared to the control side. Furthermore, the GalR1 mRNA levels decreased by 35% in the cortex of the ischemic hemisphere. The present results indicate that a stroke-induced forebrain lesion upregulates synthesis of galanin and GalR1 in the locus coeruleus, a noradrenergic cell group projecting to many forebrain areas, including cortex and the hippocampal formation. These results support the notion that galanin may play a role in the response of the central nervous system to injury and have trophic eff ects.
Place, publisher, year, edition, pages
Elsevier, 2012. Vol. 46, no 1, 19-27 p.
cerebral ischemia, galanin receptor, RT-PCR
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-68085DOI: 10.1016/j.npep.2011.11.001ISI: 000300268800003OAI: oai:DiVA.org:liu-68085DiVA: diva2:416151
On the day of the defence day the status of this article was Manuscript funding agencies|County Council of Ostergotland, Sweden||Swedish Research Council||Marianne and Marcus Wallenberg Foundation||2011-05-102011-05-102013-11-26Bibliographically approved