Kesby James P, Najera Julia A, Romoli Benedetto, Fang Yiding, Basova Liana, Birmingham Amanda, Marcondes Maria Cecilia G, Dulcis Davide, Semenova Svetlana
Department of Psychiatry, School of Medicine, University of California San Diego, La Jolla, CA, USA; Queensland Brain Institute, The University of Queensland, St. Lucia, Qld, Australia.
Department of Molecular and Cellular Neurosciences, The Scripps Research Institute, La Jolla, CA, USA.
Brain Behav Immun. 2017 Oct;65:210-221. doi: 10.1016/j.bbi.2017.05.004. Epub 2017 May 8.
Methamphetamine abuse is common among humans with immunodeficiency virus (HIV). The HIV-1 regulatory protein TAT induces dysfunction of mesolimbic dopaminergic systems which may result in impaired reward processes and contribute to methamphetamine abuse. These studies investigated the impact of TAT expression on methamphetamine-induced locomotor sensitization, underlying changes in dopamine function and adenosine receptors in mesolimbic brain areas and neuroinflammation (microgliosis). Transgenic mice with doxycycline-induced TAT protein expression in the brain were tested for locomotor activity in response to repeated methamphetamine injections and methamphetamine challenge after a 7-day abstinence period. Dopamine function in the nucleus accumbens (Acb) was determined using high performance liquid chromatography. Expression of dopamine and/or adenosine A receptors (ADORA) in the Acb and caudate putamen (CPu) was assessed using RT-PCR and immunohistochemistry analyses. Microarrays with pathway analyses assessed dopamine and adenosine signaling in the CPu. Activity-dependent neurotransmitter switching of a reserve pool of non-dopaminergic neurons to a dopaminergic phenotype in the ventral tegmental area (VTA) was determined by immunohistochemistry and quantified with stereology. TAT expression enhanced methamphetamine-induced sensitization. TAT expression alone decreased striatal dopamine (D1, D2, D4, D5) and ADORA1A receptor expression, while increasing ADORA2A receptors expression. Moreover, TAT expression combined with methamphetamine exposure was associated with increased adenosine A receptors (ADORA1A) expression and increased recruitment of dopamine neurons in the VTA. TAT expression and methamphetamine exposure induced microglia activation with the largest effect after combined exposure. Our findings suggest that dopamine-adenosine receptor interactions and reserve pool neuronal recruitment may represent potential targets to develop new treatments for methamphetamine abuse in individuals with HIV.
甲基苯丙胺滥用在感染人类免疫缺陷病毒(HIV)的人群中很常见。HIV-1调节蛋白TAT会导致中脑边缘多巴胺能系统功能障碍,这可能会导致奖赏过程受损,并促使甲基苯丙胺滥用。这些研究调查了TAT表达对甲基苯丙胺诱导的运动致敏、中脑边缘脑区多巴胺功能和腺苷受体的潜在变化以及神经炎症(小胶质细胞增生)的影响。对经强力霉素诱导在大脑中表达TAT蛋白的转基因小鼠,在反复注射甲基苯丙胺以及7天禁欲期后的甲基苯丙胺激发试验后,测试其运动活性。使用高效液相色谱法测定伏隔核(Acb)中的多巴胺功能。使用逆转录聚合酶链反应(RT-PCR)和免疫组织化学分析评估Acb和尾状壳核(CPu)中多巴胺和/或腺苷A受体(ADORA)的表达。通过微阵列和通路分析评估CPu中的多巴胺和腺苷信号传导。通过免疫组织化学确定腹侧被盖区(VTA)中非多巴胺能神经元储备池向多巴胺能表型的活动依赖性神经递质转换,并用体视学进行量化。TAT表达增强了甲基苯丙胺诱导的致敏作用。单独的TAT表达会降低纹状体多巴胺(D1、D2、D4、D5)和ADORA1A受体的表达,同时增加ADORA2A受体的表达。此外,TAT表达与甲基苯丙胺暴露相结合与腺苷A受体(ADORA1A)表达增加以及VTA中多巴胺神经元募集增加有关。TAT表达和甲基苯丙胺暴露会诱导小胶质细胞活化,联合暴露后影响最大。我们的研究结果表明,多巴胺-腺苷受体相互作用和储备池神经元募集可能是为感染HIV的个体开发甲基苯丙胺滥用新治疗方法的潜在靶点。