Hypocretin-1 causes G protein activation and increases ACh release in rat pons
dc.contributor.author | Bernard, René | en_US |
dc.contributor.author | Lydic, Ralph | en_US |
dc.contributor.author | Baghdoyan, Helen A. | en_US |
dc.date.accessioned | 2010-06-01T22:47:10Z | |
dc.date.available | 2010-06-01T22:47:10Z | |
dc.date.issued | 2003-10 | en_US |
dc.identifier.citation | Bernard, RenÉ; Lydic, Ralph; Baghdoyan, Helen A. (2003). "Hypocretin-1 causes G protein activation and increases ACh release in rat pons." European Journal of Neuroscience 18(7): 1775-1785. <http://hdl.handle.net/2027.42/75751> | en_US |
dc.identifier.issn | 0953-816X | en_US |
dc.identifier.issn | 1460-9568 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/75751 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=14622212&dopt=citation | en_US |
dc.description.abstract | The effects of the arousal-promoting peptide hypocretin on brain stem G protein activation and ACh release were examined using 16 adult Sprague-Dawley rats. In vitro [ 35 S]GTPγS autoradiography was used to test the hypothesis that hypocretin-1-stimulated G protein activation is concentration-dependent and blocked by the hypocretin receptor antagonist SB-334867. Activated G proteins were quantified in dorsal raphe nucleus (DR), locus coeruleus (LC) and pontine reticular nucleus oral part (PnO) and caudal part (PnC). Concentration–response data revealed a significant ( P < 0.001) effect of hypocretin-1 (2–2000 nm) in all brain regions examined. Maximal increases over control levels of [ 35 S]GTPγS binding were 37% (DR), 58% (LC), 52% (PnO) and 44% (PnC). SB-334867 (2 µm) significantly ( P < 0.002) blocked hypocretin-1 (200 nm)-stimulated [ 35 S]GTPγS binding in all four nuclei. This is the first autoradiographic demonstration that hypocretin-1 activates G proteins in arousal-related brain stem nuclei as a result of specific receptor interactions. This finding suggests that some hypocretin receptors in brain stem couple to inhibitory G proteins. In vivo microdialysis was used to test the hypothesis that PnO administration of hypocretin-1 increases ACh release in PnO. Dialysis delivery of hypocretin-1 (100 µm) significantly ( P < 0.002) increased (87%) ACh release. This finding is consistent with the interpretation that one mechanism by which hypocretin promotes arousal is by enhancing cholinergic neurotransmission in the pontine reticular formation. | en_US |
dc.format.extent | 361146 bytes | |
dc.format.extent | 3109 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Blackwell Science, Ltd | en_US |
dc.rights | © Federation of European Neuroscience Societies | en_US |
dc.subject.other | [ 35 S]GTPγS Autoradiography | en_US |
dc.subject.other | Dorsal Raphe Nucleus | en_US |
dc.subject.other | Locus Coeruleus | en_US |
dc.subject.other | Orexin | en_US |
dc.subject.other | REM Sleep | en_US |
dc.title | Hypocretin-1 causes G protein activation and increases ACh release in rat pons | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Anaesthesiology, University of Michigan, 7433 Medical Sciences Building I, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA | en_US |
dc.contributor.affiliationother | Pharmacology and | en_US |
dc.identifier.pmid | 14622212 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/75751/1/j.1460-9568.2003.02905.x.pdf | |
dc.identifier.doi | 10.1046/j.1460-9568.2003.02905.x | en_US |
dc.identifier.source | European Journal of Neuroscience | en_US |
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