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Nicotine-induced eeg and behavioral arousal,

dc.contributor.authorYamamoto, Ken-Ichien_US
dc.contributor.authorDomino, Edward F.en_US
dc.date.accessioned2006-04-13T14:40:17Z
dc.date.available2006-04-13T14:40:17Z
dc.date.issued1965-11en_US
dc.identifier.citationYamamoto, Ken-Ichi, Domino, Edward F. (1965/11)."Nicotine-induced eeg and behavioral arousal,." Neuropharmacology 4(6): 359-373. <http://hdl.handle.net/2027.42/31966>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B6T0C-4789MBN-7/2/ccbb8f4778f99d6e2fc153d17ddd3757en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/31966
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=5894257&dopt=citationen_US
dc.description.abstract(-) Nicotine, in doses of 0.005-0.01 mg/kg given intravenously over 1 min, produced transient behavioral arousal and EEG activation in cats with chronic indwelling brain electrodes. The effects of nicotine were evident when the animals were in natural slow wave (deep) sleep as observed behaviorally and by the EEG with recordings from various cortical and subcortical sites. After nicotine administration, the animals were aroused for a few minutes and later became sleepy behaviorally and showed EEG slow waves. This was frequently followed by activated or fast wave sleep. This phenomenon was not evident following infusion of equal volumes of warmed saline solution. In equal doses (+) nicotine, nicotine-N-oxide and cotinine did not affect EEG and behavior in slow wave sleeping cats. However, equipressor doses of (+) nicotine (0.05 mg/kg) and nicotine-N-oxide (1.5 mg/kg) produced slight behavioral and EEG arousal in cats with slow wave sleep. Massive doses of cotinine (25 mg/kg) given intravenously were less effective than (-) nicotine in doses of 0.01 mg/kg. Equipressor doses of epinephrine (E) (0.002 mg/kg), phenylalanyl lysine vasopressin (50 milliunits/kg) and DMPP (0.005 mg/kg) produced weaker EEG activation and behavioral arousal than (-) nicotine.Pretreatment with trimethidinium (2 mg/kg) prevented the cardiovascular effects of nicotine but did not alter greatly its behavioral arousal or EEG activation effects. On the other hand, mecamylamine (0.6 mg/kg) completely blocked the cardiovascular actions of nicotine as well as its effects on EEG and behavior. Larger doses of mecamylamine interfered with the natural sleep cycle of the cat. By use of such pharmacologie techniques it is concluded that the behavioral arousal and EEG desynchronizing effects of nicotine are due primarily to an action on the central nervous system rather than peripheral afferent stimulation or release of various neurohormones. However, these latter effects contribute to the total phenomenon produced by nicotine in intact animals.en_US
dc.format.extent1564319 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherElsevieren_US
dc.titleNicotine-induced eeg and behavioral arousal,en_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelPsychiatryen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbsecondlevelChemistryen_US
dc.subject.hlbsecondlevelBiological Chemistryen_US
dc.subject.hlbtoplevelScienceen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Pharmacology, University of Michigan, Ann Arbor, Michigan, U.S.A.en_US
dc.contributor.affiliationumDepartment of Pharmacology, University of Michigan, Ann Arbor, Michigan, U.S.A.en_US
dc.identifier.pmid5894257en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/31966/1/0000008.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1016/0028-3908(65)90016-Xen_US
dc.identifier.sourceNeuropharmacologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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