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Blockade of the dopaminergic neurotransmission with AMPT and reserpine induces a differential expression of genes of the dopaminergic phenotype in substantia nigra.
Neuropharmacology ( IF 4.6 ) Pub Date : 2019-12-21 , DOI: 10.1016/j.neuropharm.2019.107920
Sergio Ortiz-Padilla 1 , Elier Soto-Orduño 1 , Marisa Escobar Barrios 1 , Abril Armenta Manjarrez 1 , Yadira Bastián 2 , J Alfredo Mendez 1
Affiliation  

Dopaminergic neurons have the ability to release Dopamine from their axons as well as from their soma and dendrites. This somatodendritically-released Dopamine induces an autoinhibition of Dopaminergic neurons mediated by D2 autoreceptors, and the stimulation of neighbor GABAergic neurons mediated by D1 receptors (D1r). Here, our results suggest that the somatodendritic release of Dopamine in the substantia nigra (SN) may stimulate GABAergic neurons that project their axons into the hippocampus. Using semiquantitative multiplex RT-PCR we show that chronic blockade of the Dopaminergic neurotransmission with both AMPT and reserpine specifically decreases the expression levels of D1r, remarkably this may be the result of an antagonistic effect between AMPT and reserpine, as they induced the expression of a different set of genes when treated by separate. Furthermore, using anterograde and retrograde tracing techniques, we found that the GABAergic neurons that express D1r also project their axons in to the CA1 region of the hippocampus. Finally, we also found that the same treatment that decreases the expression levels of D1r in SN, also induces an impairment in the performance in an appetitive learning task that requires the coding of reward as well as navigational skills. Overall, our findings show the presence of a GABAergic interconnection between the SNr and the hippocampus mediated by D1r.

中文翻译:

用AMPT和利血平阻断多巴胺能神经传递可诱导黑质中多巴胺能表型基因的差异表达。

多巴胺能神经元具有从其轴突以及体细胞和树突中释放多巴胺的能力。这种体表释放的多巴胺诱导由D2自体受体介导的多巴胺能神经元的自抑制,以及由D1受体(D1r)介导的邻近GABA能神经元的刺激。在这里,我们的结果表明,黑质(SN)中多巴胺的体树突状释放可能会刺激将其轴突投射到海马中的GABA能神经元。使用半定量多重RT-PCR,我们发现AMPT和利血平均能长期阻断多巴胺能神经传递,从而特异性降低D1r的表达水平,这显然是AMPT和利血平之间产生拮抗作用的结果,因为当他们分开治疗时,它们诱导了一组不同基因的表达。此外,使用顺行和逆行追踪技术,我们发现表达D1r的GABA能神经元也将其轴突投射到海马的CA1区。最后,我们还发现,降低SN中D1r表达水平的相同治疗方法,也会在要求编码奖励和导航技能的有竞争性学习任务中导致表现受损。总体而言,我们的发现表明,SNr和D1r介导的海马之间存在GABA能互连。我们还发现,降低SN中D1r表达水平的相同治疗方法,也会在要求编码奖励和导航技能的有竞争性学习任务中导致学习成绩下降。总体而言,我们的发现表明,SNr和D1r介导的海马之间存在GABA能互连。我们还发现,降低SN中D1r表达水平的相同治疗方法,也会在要求编码奖励和导航技能的有竞争性学习任务中导致表现受损。总体而言,我们的发现表明,SNr和D1r介导的海马之间存在GABA能互连。
更新日期:2019-12-21
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