Nucleus incertus corticotrophin-releasing factor 1 receptor signalling regulates alcohol seeking in rats Walker, Leigh C., Kastman, Hanna E., Koeleman, Jan A., Smith, Craig M., Perry, Christina J., Krstew, Elena V., Gundlach, Andrew L. and Lawrence, Andrew J. 2016, Nucleus incertus corticotrophin-releasing factor 1 receptor signalling regulates alcohol seeking in rats, Addiction biology, doi: 10.1111/adb.12426. Attached Files Name Description MIMEType Size Downloads Title Nucleus incertus corticotrophin-releasing factor 1 receptor signalling regulates alcohol seeking in rats Author(s) Walker, Leigh C. Kastman, Hanna E. Koeleman, Jan A. Smith, Craig M. Perry, Christina J. Krstew, Elena V. Gundlach, Andrew L. Lawrence, Andrew J. Journal name Addiction biology Total pages 14 Publisher Wiley Place of publication Hoboken, N.J. Publication date 2016-07-20 ISSN 1369-1600 Keyword(s) alcohol corticotrophin-releasing factor nucleus incertus reinstatement relaxin-3 stress Summary Alcoholism is a chronic relapsing disorder, and stress is a key precipitant of relapse. The nucleus incertus (NI) is highly responsive to corticotrophin-releasing factor (CRF) and psychological stressors, receives a CRF innervation and expresses CRF1 and CRF2 receptor mRNA. Furthermore, the ascending NI relaxin-3 system is implicated in alcohol seeking in rats. Therefore, in alcohol-preferring rats, we examined the effect of bilateral injections into the NI of the CRF1 receptor antagonist, CP376395 or the CRF2 receptor antagonist, astressin-2B on yohimbine-induced reinstatement of alcohol seeking. Using quantitative PCR analysis of NI micropunches, we assessed the effects of chronic alcohol consumption on gene expression profiles for components of the relaxin-3 and CRF systems. Bilateral intra-NI injections of CP376395 (500 ng/0.25 µl) attenuated yohimbine-induced reinstatement of alcohol seeking. In contrast, intra-NI injections of astressin-2B (200 ng/0.25 µl) had no significant effect. In line with these data, CRF1 , but not CRF2 , receptor mRNA was upregulated in the NI following chronic ethanol intake. Relaxin family peptide 3 receptor mRNA was also increased in the NI following chronic ethanol. Our quantitative PCR analysis also identified CRF mRNA within the rat NI, and the existence of a newly identified population of CRF-containing neurons was subsequently confirmed by detection of CRF immunoreactivity in rat and mouse NI. These data suggest that NI neurons contribute to reinstatement of alcohol seeking, via an involvement of CRF1 signalling. Furthermore, chronic ethanol intake leads to neuroadaptive changes in CRF and relaxin-3 systems within rat NI. Notes In press Language eng DOI 10.1111/adb.12426 Field of Research 111708 Health and Community Services Socio Economic Objective 920414 Substance Abuse HERDC Research category C1 Refereed article in a scholarly journal ERA Research output type C Journal article Copyright notice ©2016, Society for the Study of Addiction Persistent URL http://hdl.handle.net/10536/DRO/DU:30091510 Document type: Journal Article Collection: School of Medicine Related Links Link Description Connect to Elements publication management system Go to link with your DU access privileges   Connect to published version Go to link with your DU access privileges     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. Versions Version Filter Type Fri, 24 Feb 2017, 15:04:01 EST Fri, 24 Feb 2017, 15:11:08 EST Sat, 25 Feb 2017, 04:01:13 EST Mon, 27 Feb 2017, 08:52:02 EST Thu, 02 Mar 2017, 05:06:34 EST Tue, 14 Mar 2017, 11:20:39 EST Tue, 14 Mar 2017, 11:25:43 EST Wed, 13 Sep 2017, 13:58:21 EST Wed, 13 Sep 2017, 15:07:53 EST Sat, 18 Nov 2017, 01:38:58 EST Filtered Full Citation counts:   Cited 0 times in TR Web of Science Cited 6 times in Scopus Search Google Scholar Access Statistics: 85 Abstract Views, 1 File Downloads  -  Detailed Statistics Created: Fri, 24 Feb 2017, 15:11:08 EST

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.