Expression of galanin and its receptors are perturbed in a rodent model of mild, blast-induced traumatic brain injury
2016 (English)In: Experimental Neurology, ISSN 0014-4886, E-ISSN 1090-2430, Vol. 279, 159-167 p.Article in journal (Refereed) PublishedText
The symptomatology, mood and cognitive disturbances seen in post-traumatic stress disorder (PTSD) and mild blast-induced traumatic brain injury (mbTBI) overlap considerably. However the pathological mechanisms underlying the two conditions are currently unknown. The neuropeptide galanin has been suggested to play a role in the development of stress and mood disorders. Here we applied bio- and histochemical methods with the aim to elucidate the nature of any changes in the expression of galanin and its receptors in a rodent model of mbTBI. In situ hybridization and quantitative polymerase chain reaction studies revealed significant, injury induced changes, in some cases lasting at least for one week, in the mRNA levels of galanin and/or its three receptors, galanin receptor 1-3 (GalR1-3). Such changes were seen in several forebrain regions, and the locus coeruleus. In the ventral periaqueductal gray GalR1 mRNA levels were increased, while GalR2 were decreased. Analysis of galanin peptide levels using radioimmunoassay demonstrated an increase in several brain regions including the locus coeruleus, dorsal hippocampal formation and amygdala. These findings suggest a role for the galanin system in the endogenous response to mbTBI, and that pharmacological studies of the effects of activation or inhibition of different galanin receptors in combination with functional assays of behavioral recovery may reveal promising targets for new therapeutic strategies in mbTBI. (C) 2016 Elsevier Inc. All rights reserved.
Place, publisher, year, edition, pages
ACADEMIC PRESS INC ELSEVIER SCIENCE , 2016. Vol. 279, 159-167 p.
Anxiety; Cholecystokinin (CCK); Depression; Neuropeptide; Periaqueductal gray; Receptor; Transcriptional regulation; Translational regulation; Transmitter coexistence
IdentifiersURN: urn:nbn:se:liu:diva-128142DOI: 10.1016/j.expneurol.2016.02.019ISI: 000374612900014PubMedID: 26928087OAI: oai:DiVA.org:liu-128142DiVA: diva2:929611
Funding Agencies|Swedish Armed Forces RD [AF.9221006]; Swedish Research Council [04X-2887]; Karolinska Institutet Funds2016-05-192016-05-192016-05-19