Antagonization of clonidine- and morphine-promoted antinociception by kainic acid lesion of nucleus reticularis gigantocellularis in the rat

Content Provider	Semantic Scholar
Author	Lai, Yuan-Yang Chan, Samuel H. H.
Copyright Year	1982
Abstract	Abstract We evaluated the participation of nucleus reticularis gigantocellularis (NRGC) in clonidine- and morphine-induced analgesia in young rats, using the hot-plate assay as the nociceptive test. Bilateral kainic acid lesion of the NRGC did not alter the baseline pain responses to noxious heat stimulus. Selective destruction of the NRGC neuronal perikarya, however, significantly attenuated the analgesic efficacy of an optimal dose of clonidine or morphine. Sham-lesion animals, on the other hand, showed no appreciable alteration in the antinociceptive potency of both the imidazoline compound and the opiate. We conclude that the NRGC may be a critical central site for clonidine- and morphine-promoted pain inhibition, although this reticular nucleus did not appear to function as a tonically active endogenous analgesic mechanism. The incomplete elimination of morphine-elicited antinociception by NRGC lesion confirmed the engagement of other neural substrates in the process. We discuss whether NRGC participates in pain suppression by the opiate in parallel or in series to these other central sites.
Starting Page	38
Ending Page	45
Page Count	8
File Format	PDF HTM / HTML
DOI	10.1016/0014-4886(82)90187-X
PubMed reference number	7117484
Journal	Medline
Volume Number	78
Alternate Webpage(s)	https://api.elsevier.com/content/article/pii/001448868290187X
Alternate Webpage(s)	https://www.sciencedirect.com/science/article/pii/001448868290187X?dgcid=api_sd_search-api-endpoint
Alternate Webpage(s)	https://doi.org/10.1016/0014-4886%2882%2990187-X
Journal	Experimental Neurology
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article