Abstract:
Neuroscientists and psychiatrists working in the areas of \"pain and addiction\" are asked in this perspective article to reconsider the current use of dopaminergic blockade (like chronic opioid agonist therapy), and instead to consider induction of dopamine homeostasis by putative pro-dopamine regulation. Pro-dopamine regulation could help pharmaceutical opioid analgesic agents to mitigate hypodopaminergia-induced hyperalgesia by inducing transmodulation of dopaminergic signaling. An optimistic view is that early predisposition to diagnosis based on genetic testing, (pharmacogenetic/pharmacogenomic monitoring), combined with appropriate urine drug screening, and treatment with pro-dopamine regulators, could conceivably reduce stress, craving, and relapse, enhance well-being and attenuate unwanted hyperalgesia. These concepts require intensive investigation. However, based on the rationale provided herein, there is a good chance that combining opioid analgesics with genetically directed pro-dopamine-regulation using KB220 (supported by 43 clinical studies). This may become a front-line technology with the potential to overcome, in part, the current heightened rates of chronic opioid-induced hyperalgesia and concomitant Reward Deficiency Syndrome (RDS) behaviors. Current research does support the hypothesis that low or hypodopaminergic function in the brain may predispose individuals to low pain tolerance or hyperalgesia.
摘要:
在这篇观点文章中,在“疼痛和成瘾”领域工作的神经科学家和精神病学家被要求重新考虑目前使用多巴胺能阻滞(如慢性阿片类激动剂治疗),而是考虑通过推定的前多巴胺调节来诱导多巴胺稳态。多巴胺前调节可以通过诱导多巴胺能信号的转换来帮助药物阿片类镇痛药减轻多巴胺引起的痛觉过敏。一个乐观的观点是,基于基因检测的早期诊断倾向,(药物遗传学/药物基因组学监测),结合适当的尿液药物筛选,用前多巴胺调节剂治疗,可以想象减轻压力,渴望,和复发,增强健康和减轻不必要的痛觉过敏。这些概念需要深入调查。然而,根据本文提供的基本原理,使用KB220将阿片类镇痛药与遗传指导的多巴胺前调节相结合的可能性很大(得到43项临床研究的支持).这可能成为一线技术,有可能克服,在某种程度上,目前,慢性阿片类药物诱导的痛觉过敏和伴随的奖励缺乏综合征(RDS)行为的发生率升高。当前的研究确实支持以下假设:大脑中的多巴胺能功能低下或低多巴胺能功能可能使个体易患低疼痛耐受性或痛觉过敏。