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Supraspinal nocifensive responses of cats: Spinal cord pathways, monoamines, and modulation

dc.contributor.authorCasey, Kenneth L.en_US
dc.contributor.authorMorrow, Thomas J.en_US
dc.date.accessioned2007-04-06T18:20:52Z
dc.date.available2007-04-06T18:20:52Z
dc.date.issued1988-04-22en_US
dc.identifier.citationCasey, Kenneth L.; Morrow, Thomas J. (1988)."Supraspinal nocifensive responses of cats: Spinal cord pathways, monoamines, and modulation." The Journal of Comparative Neurology 270(4): 591-605. <http://hdl.handle.net/2027.42/50039>en_US
dc.identifier.issn0021-9967en_US
dc.identifier.issn1096-9861en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/50039
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=2897383&dopt=citationen_US
dc.description.abstractThese experiments were conducted to determine (1) whether dorsal and ventral ascending spinal pathways can each mediate unlearned supraspinal nocifensive responses of cats to noxious thermal stimuli and (2) whether interrupting the spinal projection of supraspinal monoaminergic neurons alters the excitability and natural modulation of these responses. In partially restrained cats, thermal pulses (≥ 47°C) delivered to the hindlimbs of intact cats or rostral to lesions of the thoracic spinal cord elicited abrupt body movements and interruption of eating (or of exploring for) liquified food. These electronically monitored responses automatically terminated the stimulus. Natural modulation of responsiveness was produced by delivering food and thermal stimuli simultaneously; this reduced response probability by an average of 41%. Complete transection of the thoracic spinal cord eliminated both thermally elicited responses, and orienting responses to noxious and tactile mechanical stimulation of the hindlimbs. Ventral bilateral thoracic spinal cord lesions that spared only the dorsal funiculus and portions of the dorsolateral funiculus (three cats) significantly reduced orienting responses to all mechanical hindlimb stimuli and reduced, but did not eliminate, movement and interrupt responses to noxious thermal hindlimb stimuli. Response latency was unaffected. Food-induced response supression persisted although lumbar spinal cord concentrations of serotonin (5HT) and norepinephrine (NE) were markedly reduced. A bilateral lesion of the dorsal funiculi and dorsal portions of the dorsolateral funiculi (one cat) also reduced nocifensive responsiveness, but only the NE concentration in lumbar spinal cord was reduced significantly relative to a matched cervical sample. In contrast, deep bilateral lesions of the dorsolateral funiculi (two cats) produced an increase in the probability of movement and interrupt responses without affecting either response latency or food-induced response supression. Lumbar spinal cord concentrations of NE and, in one cat, 5HT were reduced. We conclude that (1) the dorsal and ventral spinal funiculi are each sufficient to initiate and necessary to maintain normal supraspinally organized nocifensive behavior in the cat; (2) descending monoaminergic pathways are not necessary for the phasic modulation of these responses; and (3) the tonic excitability, but not the phasic modulation, of these responses is determined in part by fibers in the dorsolateral funiculus.en_US
dc.format.extent1730977 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherAlan R. Liss, Inc.en_US
dc.publisherWiley Periodiocals, Inc.en_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology and Psychiatryen_US
dc.titleSupraspinal nocifensive responses of cats: Spinal cord pathways, monoamines, and modulationen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDeparment of Neurology, University of Michigan, Neurology Research Laboratories (Neurophysiology), Veterans Administration Medical Center, Ann Arbor, Michigan 48105 ; Deparment of Physiology, University of Michigan, Neurology Research Laboratories (Neurophysiology), Veterans Administration Medical Center, Ann Arbor, Michigan 48105en_US
dc.contributor.affiliationumDeparment of Neurology, University of Michigan, Neurology Research Laboratories (Neurophysiology), Veterans Administration Medical Center, Ann Arbor, Michigan 48105en_US
dc.identifier.pmid2897383en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/50039/1/902700412_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/cne.902700412en_US
dc.identifier.sourceThe Journal of Comparative Neurologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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