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- W1889480724 abstract "The neurochemical and functional correlates of opioid receptor up-regulation after chronic antagonist administration in vivo and of down-regulation after withdrawal of antagonist were examined. Total brain opioid receptors increased 1.9-fold by day 8 of naltrexone administration, after which no further increase was observed; the newly synthesized or unmasked receptors exhibited an enhanced sensitivity to guanyl nucleotide modulation. Withdrawal from chronic naltrexone treatment resulted in a return to nearly control levels of receptor density and guanyl nucleotide sensitivity in a period of 6 days. These results suggest that up-regulation is accompanied by an increased coupling of the receptors to the inhibitory guanyl nucleotide binding protein (Ni) and that down-regulation involves the dissociation of the receptor/Ni complex. In experiments designed to target opiate receptor subtypes, long-term treatment with naltrexone was found to produce a coordinated up-regulation of brain mu and delta receptors, but did not cause a significant change in the density or affinity of kappa or sigma receptors. These findings indicate that the kappa and sigma opiate receptor classes may be subject to independent control mechanisms. Chronic naltrexone treatment also resulted in an enhanced morphine-induced analgesia. This result indicates that a functional supersensitivity occurs as a result of the selective up-regulation of mu and delta receptors. After withdrawal from naltrexone, supersensitivity to morphine-induced analgesia decreased monotonically and, in parallel to opioid receptor density, to prenaltrexone treatment levels within 6 days. Together, these results suggest a functional significance for antagonist-induced mu and delta opiate receptor up-regulation." @default.
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- W1889480724 title "Neurochemical and functional correlates of naltrexone-induced opiate receptor up-regulation." @default.
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