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William A. Corrigall Mary Ann Linseman RoseMarie D'Onofrio Hau Lei 《Psychopharmacology》1986,89(3):327-333
A previously reported paradigm in which rats run down a runway for food reward followed by morphine injection was analyzed to assess the utility of the paradigm in studies of opiate reinforcement. One experiment replicated the original report that post-trial morphine caused both an increase in runway speed and a decrease in food consumption (taste aversion) over successive trials, and showed in addition that the increase in runway speed did not occur as a result of food deprivation alone, but required the animals to have consumed food in the goal box. A second study using the quaternary opiate antagonist methyl naltrexone to block the peripheral effects of morphine suggested that the increase in runway speed has a peripheral locus while the taste aversion has a central one. A third experiment in which morphine was microinjected into either the lateral ventricle or the ventral tegmental area supported these observations, in that intracranial morphine failed to result in an increased runway speed, but did produce taste aversion after microinjection into either site. These findings also suggest that the increase in runway speed caused by post-trial morphine in this experiment has a peripheral locus of effect, which is probably distinct from the central effect that supports morphine self-administration and conditioned place preference.
Offprint requests to: W.A.CorrigallThe views expressed in this publication are those of the authors and do not necessarily reflect those of the Addiction Research Foundation 相似文献
3.
Naltrexone-3-salicylate (3), a prodrug of naltrexone (1), was prepared by a simple procedure from naltrexone-3-acetylsalicylate (2). The plasma (dog and human) hydrolysis half-life of 3 was found to be approximately 30 min. Compound 2 was previously shown to hydrolyze in dog and human plasma with a fast deacetylation step to 3, followed by slower hydrolysis of 3 to 1 (t
1/2, 30 min). Oral naltrexone bioavailability was greatly improved (30-fold) after oral administration of 3 to dogs, similar to the improvement observed after oral administration of 2. The half-life of naltrexone in dogs after oral administration of 3 was similar to that observed after oral administration of 2 (1 hr). 相似文献
4.
Morphine-6beta-glucuronide modulates the expression of inducible nitric oxide synthase 总被引:1,自引:0,他引:1
The immunomodulatory effects of morphine are well established; however, suprisingly little is known about the immunomodulatory properties of the major metabolites of morphine. The present study tests the hypothesis that expression of inducible nitric oxide synthase (iNOS) is modulated by the administration of the morphine metabolite, morphine-6-glucuronide. The initial study using rats shows that morphine-6-glucuronide administration (0, 1.0, 3.163, 10 mg/kg s.c.) results in a pronounced reduction in lipopolysaccharide (LPS)-induced expression of iNOS (inducible nitricoxide synthease) in spleen, lung, and liver tissue as measured by western blotting. Morphine-6-glucuronide also produces a reduction in the level of plasma nitrite/nitrate, the more stable end-product of nitric oxide degradation. In a subsequent study, administration of the opioid receptor antagonist, naltrexone (0.1 mg/kg) prior to the injection of morphine-6-glucuronide (10 mg/kg) blocks the morphine-6-glucuronide induced reduction of iNOS expression and plasma nitrite/nitrite levels indicating that the effect is mediated via the opioid-receptor. This study provides the first evidence that morphine-6-glucuronide alters the expression of iNOS. 相似文献
5.
院外纳曲酮治疗酒精依赖的疗效观察 总被引:3,自引:0,他引:3
目的 :评估纳曲酮院外治疗酒依赖的临床疗效。方法 :采用随机对照的方法 ,分别对纳曲酮组和安慰剂组各 2 3例和 2 2例 ,作总疗程 12周的临床观察。结果 :纳曲酮显著降低病人对酒精的渴求程度 ,其疗后 4、 8、 12周的保持率分别为 91 3 %、 77 9%、 73 3 % ,明显高于安慰剂。纳曲酮的副作用与安慰剂相当 ,其主要副作用为轻度的恶心、厌食、头晕。结论 :纳曲酮是一种安全有效的治疗酒依赖的药物 相似文献
6.
Methadone is currently the only opioid available for the pharmacotherapy of opioid dependence. Cross-tolerance between methadone and other opioids constitutes the pharmacological basis for substitution and attenuating the effects of illicit opioid use. However, these principles limit the utility of methadone. Potential alternative opioids include long-acting partial agonists such as buprenorphine and pure antagonists such as naltrexone. Buprenorphine is an alternative to methadone with intermediate intrinsic efficacy. It has a large margin of safety, yet displays some agonist actions similar to methadone. It has greater potential than methadone to safely and effectively block the actions of illicit opioids. Naltrexone is a safe, convenient opioid-antagonist for use following detoxification from opioid agonists. Its main use is to block the actions of other opioids, thereby attenuating or eliminating illicit use during treatment. However, it is poorly accepted by many clients, limiting its application to a sub-group who are highly motivated to detoxify. The distinct pharmacological properties of these opioids can overcome some of the drawbacks of methadone, but other limitations may emerge. Non-opioid adjuncts such as alpha2-adrenoceptor agonists can also have a role during detoxification. These drugs might be of use for specific groups of opioid users, providing therapists with the flexibility to tailor pharmacotherapy to the individual needs of clients. 相似文献
7.
Robert G. Brzyski M.D. Ph.D. Amabel Viniegra M.D. David F. Archer M.D. 《Fertility and sterility》1997,68(5):855-859
Objective: To investigate whether establishment and maintenance of chronic opioid blockade throughout the follicular phase of the menstrual cycle influences midcycle and luteal phase prolactin levels.Design: Randomized, double-blind, crossover study.Setting: Academic research environment.Patient(s): Volunteers, aged 21–35 years, with regular menstrual cycles.Intervention(s): Naltrexone (50 mg) or placebo were administered on cycle days 2–14. Blood samples were obtained in the early follicular phase and in the periovulatory and midluteal phases of the menstrual cycle.Main Outcome Measure(s): Serum prolactin levels.Result(s): In the early follicular phase, serum prolactin levels were equivalent in naltrexone (12.0 ± 2.7 μg/L; mean ± SE) and placebo (12.1 ± 2.9 ug/L) cycles. A statistically significant increase in serum prolactin was observed on the day of the LH surge (naltrexone: 22.6 ± 3.7 μg/L; placebo: 21.7 ± 2.7 μg/L; P < 0.05 versus early follicular phase), but no difference between treatments was observed. However, midluteal prolactin levels were statistically significantly lower in naltrexone cycles compared with placebo cycles (12.6 ± 3.3 versus 15.4 ± 3.0 )ug/L; P < 0.05).Conclusion(s): Chronic blockade of opioid activities during the follicular phase does not affect midcycle prolactin increments, but withdrawal of opioid blockade may enhance opioid effects on prolactin levels in the luteal phase. 相似文献
8.
Yu-Syuan Wang Tsai-Wei Hung Eun-Kyung Bae Kuo-Jen Wu Wei Hsieh Seong-Jin Yu 《CNS Neuroscience & Therapeutics》2021,27(7):831-841
AimsNaltrexone is a mu opioid receptor (MOR) antagonist used to treat drug dependence in patients. Previous reports indicated that MOR antagonists reduced neurodegeneration and inflammation after brain injury. The purpose of this study was to evaluate the neuroprotective effect of naltrexone in cell culture and a mouse model of traumatic brain injury (TBI).MethodsThe neuroprotective effect of naltrexone was examined in primary cortical neurons co‐cultured with BV2 microglia. Controlled cortical impact (CCI) was delivered to the left cerebral cortex of adult male MOR wild‐type (WT) and knockout (KO) mice. Naltrexone was given daily for 4 days, starting from day 2 after lesioning. Locomotor activity was evaluated on day 5 after the CCI. Brain tissues were collected for immunostaining, Western, and qPCR analysis.ResultsGlutamate reduced MAP2 immunoreactivity (‐ir), while increased IBA1‐ir in neuron/BV2 co‐culture; both responses were antagonized by naltrexone. TBI significantly reduced locomotor activity and increased the expression of IBA1, iNOS, and CD4 in the lesioned cortex. Naltrexone significantly and equally antagonized the motor deficits and expression of IBA1 and iNOS in WT and KO mice. TBI‐mediated CD4 protein production was attenuated by naltrexone in WT mice, but not in KO mice.ConclusionNaltrexone reduced TBI‐mediated neurodegeneration and inflammation in MOR WT and KO mice. The protective effect of naltrexone involves non‐MOR and MOR mechanisms. 相似文献
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