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Psychostimulant use disorder emphasizing methamphetamine and the opioid -dopamine connection: Digging out of a hypodopaminergic ditch
Journal of the Neurological Sciences ( IF 3.6 ) Pub Date : 2021-01-01 , DOI: 10.1016/j.jns.2020.117252
Kenneth Blum , Jean Lud Cadet , Mark S. Gold

BACKGROUND Approved food and drug administration (FDA) medications to treat Psychostimulant Use Disorder (PUD) are needed. Both acute and chronic neurological deficits related to the neurophysiological effects of these powerfully addictive drugs can cause stroke and alterations in mood and cognition. OBJECTIVE This article presents a brief review of the psychiatric and neurobiological sequelae of methamphetamine use disorder, some known neurogenetic associations impacted by psychostimulants, and explores treatment modalities and outcomes. HYPOTHESIS The authors propose that gentle D2 receptor stimulation accomplished via some treatment modalities can induce dopamine release, causing alteration of D2-directed mRNA and thus enhanced function of D2 receptors in the human. This proliferation of D2 receptors, in turn, will induce the attenuation of craving behavior, especially in genetically compromised high-risk populations. DISCUSSION A better understanding of the involvement of molecular neurogenetic opioid, mesolimbic dopamine, and psychostimulant connections in "wanting" supports this hypothesis. While both scientific and, clinical professionals search for an FDA approved treatment for PUD the induction of dopamine homeostasis, via activation of the brain reward circuitry, offers treatment for underlying neurotransmitter functional deficits, potential prophylaxis, and support for recovery efforts. CONCLUSION Dopamine regulation may help people dig out of their hypodopaminergia ditch.

中文翻译:

强调甲基苯丙胺和阿片类药物-多巴胺联系的精神兴奋剂使用障碍:挖出低多巴胺能沟

背景 需要经批准的食品和药物管理局 (FDA) 药物来治疗精神兴奋剂使用障碍 (PUD)。与这些强效成瘾药物的神经生理学效应相关的急性和慢性神经功能缺损都可能导致中风以及情绪和认知的改变。目的 本文简要回顾了甲基苯丙胺使用障碍的精神和神经生物学后遗症、一些已知的受精神兴奋剂影响的神经遗传学关联,并探讨了治疗方式和结果。假设 作者提出,通过某些治疗方式实现的温和 D2 受体刺激可以诱导多巴胺释放,导致 D2 导向 mRNA 的改变,从而增强人类 D2 受体的功能。这种 D2 受体的增殖,反过来,会导致渴求行为的减弱,特别是在基因受损的高危人群中。讨论 更好地了解分子神经发生阿片类药物、中脑边缘多巴胺和精神兴奋剂在“想要”中的联系支持了这一假设。虽然科学和临床专业人士都在寻找 FDA 批准的 PUD 治疗方法,但通过激活大脑奖励回路来诱导多巴胺稳态,为潜在的神经递质功能缺陷提供治疗、潜在的预防和支持恢复工作。结论 多巴胺调节可以帮助人们摆脱多巴胺缺乏症的困扰。中脑边缘多巴胺和“想要”中的精神兴奋剂连接支持这一假设。虽然科学和临床专业人士都在寻找 FDA 批准的 PUD 治疗方法,但通过激活大脑奖励回路来诱导多巴胺稳态,为潜在的神经递质功能缺陷提供治疗、潜在的预防和支持恢复工作。结论 多巴胺调节可以帮助人们摆脱多巴胺缺乏症的困扰。中脑边缘多巴胺和“想要”中的精神兴奋剂连接支持这一假设。虽然科学和临床专业人士都在寻找 FDA 批准的 PUD 治疗方法,但通过激活大脑奖励回路来诱导多巴胺稳态,为潜在的神经递质功能缺陷提供治疗、潜在的预防和支持恢复工作。结论 多巴胺调节可以帮助人们摆脱多巴胺缺乏症的困扰。潜在的预防措施,并支持恢复工作。结论 多巴胺调节可以帮助人们摆脱多巴胺缺乏症的困扰。潜在的预防措施,并支持恢复工作。结论 多巴胺调节可以帮助人们摆脱多巴胺缺乏症的困扰。
更新日期:2021-01-01
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