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naltrexone may up-regulate endogenous opioid receptors

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that is basically what this study from pubmed.com says :

Reduction of alcohol drinking and upregulation of opioid receptors

by oral naltrexone in AA rats.

Parkes H, Sinclair JD.

Department of Mental Health and Alcohol Research, National Public

Health Institute, POB 719, FIN-00101, Helsinki, Finland.

Rats of the high-drinking AA line were given 1 mg/kg naltrexone

(NTX) or vehicle orally with a stress-free procedure just before 1 h

of access to 10% ethanol daily for 8 days and again, 8 h later on

the first 7 days. Forebrain homogenate binding studies using 0.03-

6.00 nM [3H] naloxone were conducted from 1 to 4 days following

treatment. NTX significantly suppressed alcohol intake, with the

effect becoming progressively greater over days and continuing

during the post-treatment period. Saturation binding studies in

brain homogenate revealed that NTX had increased the B(max) for

opioid receptors by 93%, 74%, 49%, and 28%, respectively, from post-

treatment days 1 to 4 without altering K(d). B(max) was negatively

correlated (r=-0.510, p=0.008) with alcohol intake during the

preceding hour, but in control rats, it was positively correlated

with changes in alcohol intake over time (r=+0.790, p=0.020). These

results are consistent with the hypothesis that opioid receptors

mediate reinforcement from alcohol and that NTX reduces subsequent

alcohol drinking by extinction. Opioid receptor upregulation can

develop simultaneously with suppression of drinking and may

partially counteract the clinical benefits from NTX in the treatment

of alcoholism.

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