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1 centers mediating the antipruritic effect of butorphanol.
3 ndent by intracerebroventricular infusion of butorphanol (26 nmol microliter-1 h-1) via osmotic minip
4 been intracerebroventricularly infused with butorphanol (26 nmol/1 microl/h) or U-69,593 (26 nmol/10
5 imine (nor-BNI)-precipitated withdrawal from butorphanol, (5alpha,7alpha,8beta)-(+)-N-methyl-N-[7-(1-
6 NTI did not reduce the orexigenic effects of butorphanol, an agonist that binds to both kappa- and mu
7 t were involved in the inhibition of itch by butorphanol and could represent potential targets for th
8 rphine > DAMGO = beta-endorphin > morphine > butorphanol, and the affinity of DAMGO in alkaloid- but
10 rphine, DAMGO, beta-endorphin, morphine, and butorphanol, DAMGO-stimulated GTP[gamma-35S] binding was
11 tem is more susceptible to alteration during butorphanol dependence than is the adenylate cyclase sys
12 evels of glutamate in the LC of morphine- or butorphanol-dependent rats measured by in vivo microdial
13 binge eating to control levels, and although butorphanol did not trigger chow binge eating, it enhanc
15 re prominent by 7 h after discontinuation of butorphanol infusion and suggest that NMDA binding sites
20 sed with 26 nmol/microliter/h of morphine or butorphanol intracerebroventricularly (i.c.v.) via osmot
21 e examined the effect of mixed-action opioid butorphanol on histamine itch, cowhage itch, and heat pa
22 Influences of continuous administration of butorphanol on the autoradiography of [3H]glutamate bind
25 e levels in the LC markedly increased in the butorphanol- or U-69,593-dependent rats within 60 min fo
26 observed following nor-BNI challenge in the butorphanol- or U-69,593-infused rats, with only minimal
30 tic and orexigenic responses to naloxone and butorphanol, respectively, and by testing the ability of
32 respectively, and by testing the ability of butorphanol to elicit binge eating of chow when palatabl
33 vealed that the reduction in cowhage itch by butorphanol was correlated with changes in cerebral perf
36 ntly kappa-opioid analgesics, nalbuphine and butorphanol; was compared in males and females who under
37 results demonstrate that the development of butorphanol withdrawal is more prominent by 7 h after di
39 ay more important role in the development of butorphanol withdrawal than that of channel blocking sit
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