THE EFFECTS OF PROTECTION BY D-PEN(2)-D-PEN(5)-ENKEPHALIN OR D-ALA(2)-NMEPHE(4)-GLY-OL-ENKEPHALIN AGAINST BETA-CHLORNALTREXAMINE IN THE SPINAL GORD ON THE ANTINOCICEPTION INDUCED BY BETA-ENDORPHIN ADMINISTEREDINTRACEREBROVENTRICULARLY IN THE MOUSE

Citation
Hw. Shu et al., THE EFFECTS OF PROTECTION BY D-PEN(2)-D-PEN(5)-ENKEPHALIN OR D-ALA(2)-NMEPHE(4)-GLY-OL-ENKEPHALIN AGAINST BETA-CHLORNALTREXAMINE IN THE SPINAL GORD ON THE ANTINOCICEPTION INDUCED BY BETA-ENDORPHIN ADMINISTEREDINTRACEREBROVENTRICULARLY IN THE MOUSE, Neuropeptides, 27(2), 1994, pp. 143-149
Citations number
29
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism
Journal title
ISSN journal
01434179
Volume
27
Issue
2
Year of publication
1994
Pages
143 - 149
Database
ISI
SICI code
0143-4179(1994)27:2<143:TEOPBD>2.0.ZU;2-2
Abstract
Chlornaltrexamine (beta-CNA, 0.5 mu g) alone or beta-CNA plus either m u-agonist, D-Ala(2)-NMePhe(4)-Gly-ol -enkephalin (DAMGO, 500 ng) or de lta-agonist, D-Pen(2)-D-Pen(5)-enkephalin (DPDPE, 10 mu g) was injecte d intrathecally (i.t.) to protect mu- or delta-opioid receptors, respe ctively, for 24 h in male ICR mice. The antinociception was assessed b y the tail-flick and hot-plate test. DPDPE or DAMGO injected i.t. incr eased inhibition of the tail-flick and hot-plate response in a dose-de pendent man ner. The dose-response curve for tail-flick and hot-plate response induced by DPDPE or DAMGO in i.t. saline-treated group signif icantly shifted to the right in i.t. beta-CNA alone treated group but returned to the control level in the group treated with i.t. beta-CNA coadministered with DPDPE or DAMGO, respectively. The effects of prote ction of mu- and delta-opioid receptor in the spinal cord on inhibitio n of the tail-flick and hot-plate response induced by beta-endorphin a nd morphine administered intracerebroventricularly (i.c.v.) were then studied. Intrathecal pretreatment with beta-CNA or beta-CNA coadminist ered with DAMGO attenuated inhibition of the tail-flick response induc ed by beta-endorphin administered i.c.v. However, i.t. treatment with beta-CNA coadministered with DPDPE did not affect inhibition of the ta il-flick response induced by beta-endorphin administered i.c.v. Intrat hecal pretreatment with beta-CNA or PCNA coadministered with either DP DPE or DAMGO did not alter inhibition of the hot-plate response induce d by beta-endorphin administered i.c.v. Intrathecal injection of beta- CNA alone did not affect inhibition of the tail-flick and hot-plate re sponse induced by morphine given i.c.v. The results suggest that spina l delta- but not mu-opioid receptors are involved in inhibition of the tail-flick response induced by beta-endorphin given i.c.v. On the oth er hand, inhibition of the tail-flick and hot-plate response induced b y morphine given i.c.v. is not mediated through spinal opioid receptor s.