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
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
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.