Tanda Gianluigi, Mereu Maddalena, Hiranita Takato, Quarterman Juliana C, Coggiano Mark, Katz Jonathan L
Medication Development Program, Molecular Targets and Medication Discovery Branch, NIDA-IRP, NIH/DHHS, Baltimore, MD, USA.
Psychobiology Section, Molecular Neuropsychiatry Research Branch, NIDA-IRP, NIH/DHHS, Baltimore, MD, USA.
Neuropsychopharmacology. 2016 Oct;41(11):2772-81. doi: 10.1038/npp.2016.91. Epub 2016 Jun 14.
Effective medications for drug abuse remain a largely unmet goal in biomedical science. Recently, the (+)-enantiomers of naloxone and naltrexone, TLR4 antagonists, have been reported to attenuate preclinical indicators of both opioid and stimulant abuse. To further examine the potential of these compounds as drug-abuse treatments, we extended the previous assessments to include a wider range of doses and procedures. We report the assessment of (+)-naloxone and (+)-naltrexone on the acute dopaminergic effects of cocaine and heroin determined by in vivo microdialysis, on the reinforcing effects of cocaine and the opioid agonist, remifentanil, tested under intravenous self-administration procedures, as well as the subjective effects of cocaine determined by discriminative-stimulus effects in rats. Pretreatments with (+)-naloxone or (+)-naltrexone did not attenuate, and under certain conditions enhanced the stimulation of dopamine levels produced by cocaine or heroin in the nucleus accumbens shell. Furthermore, although an attenuation of either cocaine or remifentanil self-administration was obtained at the highest doses of (+)-naloxone and (+)-naltrexone, those doses also attenuated rates of food-maintained behaviors, indicating a lack of selectivity of TLR4 antagonist effects for behaviors reinforced with drug injections. Drug-discrimination studies failed to demonstrate a significant interaction of (+)-naloxone with subjective effects of cocaine. The present studies demonstrate that under a wide range of doses and experimental conditions, the TLR4 antagonists, (+)-naloxone and (+)-naltrexone, did not specifically block neurochemical or behavioral abuse-related effects of cocaine or opioid agonists.
有效的药物滥用治疗药物在生物医学领域仍是一个尚未实现的目标。最近,据报道,纳洛酮和纳曲酮的(+)-对映体(TLR4拮抗剂)可减轻阿片类药物和兴奋剂滥用的临床前指标。为进一步研究这些化合物作为药物滥用治疗药物的潜力,我们扩展了先前的评估,纳入了更广泛的剂量和程序。我们报告了(+)-纳洛酮和(+)-纳曲酮对可卡因和海洛因急性多巴胺能效应的评估(通过体内微透析测定)、对可卡因和阿片类激动剂瑞芬太尼强化效应的评估(在静脉自我给药程序下测试),以及对可卡因在大鼠中通过辨别刺激效应确定的主观效应的评估。用(+)-纳洛酮或(+)-纳曲酮预处理并未减轻,且在某些条件下增强了可卡因或海洛因在伏隔核壳中产生的多巴胺水平刺激。此外,尽管在(+)-纳洛酮和(+)-纳曲酮的最高剂量下获得了可卡因或瑞芬太尼自我给药的减轻,但这些剂量也降低了食物维持行为的速率,表明TLR4拮抗剂对药物注射强化行为的效应缺乏选择性。药物辨别研究未能证明(+)-纳洛酮与可卡因主观效应之间存在显著相互作用。本研究表明,在广泛的剂量和实验条件下,TLR4拮抗剂(+)-纳洛酮和(+)-纳曲酮并未特异性阻断可卡因或阿片类激动剂与神经化学或行为滥用相关的效应。