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Hypocretin-1 causes G protein activation and increases ACh release in rat pons

dc.contributor.authorBernard, Renéen_US
dc.contributor.authorLydic, Ralphen_US
dc.contributor.authorBaghdoyan, Helen A.en_US
dc.date.accessioned2010-06-01T22:47:10Z
dc.date.available2010-06-01T22:47:10Z
dc.date.issued2003-10en_US
dc.identifier.citationBernard, 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.issn0953-816Xen_US
dc.identifier.issn1460-9568en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/75751
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=14622212&dopt=citationen_US
dc.description.abstractThe 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
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dc.publisherBlackwell Science, Ltden_US
dc.rights© Federation of European Neuroscience Societiesen_US
dc.subject.other[ 35 S]GTPγS Autoradiographyen_US
dc.subject.otherDorsal Raphe Nucleusen_US
dc.subject.otherLocus Coeruleusen_US
dc.subject.otherOrexinen_US
dc.subject.otherREM Sleepen_US
dc.titleHypocretin-1 causes G protein activation and increases ACh release in rat ponsen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumAnaesthesiology, University of Michigan, 7433 Medical Sciences Building I, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USAen_US
dc.contributor.affiliationotherPharmacology anden_US
dc.identifier.pmid14622212en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/75751/1/j.1460-9568.2003.02905.x.pdf
dc.identifier.doi10.1046/j.1460-9568.2003.02905.xen_US
dc.identifier.sourceEuropean Journal of Neuroscienceen_US
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