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首页> 外文期刊>The European Journal of Neuroscience >Suppression of excitatory cholinergic synaptic transmission by Drosophila dopamine D1-like receptors.
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Suppression of excitatory cholinergic synaptic transmission by Drosophila dopamine D1-like receptors.

机译：果蝇多巴胺D1样受体抑制兴奋性胆碱能突触传递。

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摘要

The physiological function of dopamine is mediated through its G-protein-coupled receptor family. In Drosophila, four dopamine receptors have been molecularly characterized so far. However, due largely to the absence of a suitable preparation, the role of Drosophila dopamine receptors in modulating central synaptic transmission has not been examined. The present study investigated mechanisms by which dopamine modulates excitatory cholinergic synaptic transmission in Drosophila using primary neuronal cultures. Whole-cell recordings demonstrated that cholinergic excitatory postsynaptic currents (EPSCs) were down-regulated by focally applied dopamine (10-500 microm). The vertebrate D1 specific agonists SKF38393 and 6-chloro-APB (10 microm) mimicked dopamine-mediated suppression of cholinergic synaptic transmission with higher potency. In contrast, the D2 agonists quinpirole and bromocriptine did not alter cholinergic EPSCs, demonstrating that dopamine-mediated suppression of cholinergic synaptic transmission is specifically through activation of Drosophila D1-like receptors. Biophysical analysis of miniature EPSCs indicated that cholinergic suppression by activation of D1-like receptors is presynaptic in origin. Dopamine modulation of cholinergic transmission is not mediated through the cAMP/protein kinase A signaling pathway as cholinergic suppression by dopamine occurred in the presence of the protein kinase A inhibitor H-89. In addition, an adenylate cyclase activator, forskolin, led to an increase, not a decrease, of cholinergic EPSC frequency. Finally, we showed that activation of D1-like receptors decreased the frequency of action potentials in cultured Drosophila neurons by inhibiting excitatory cholinergic transmission. All our data demonstrated that activation of D1-like receptors in Drosophila neurons negatively modulates excitatory cholinergic synaptic transmission and thus inhibits neuronal excitability.
机译：多巴胺的生理功能通过其G蛋白偶联受体家族介导。迄今为止，在果蝇中，已经对四种多巴胺受体进行了分子表征。然而，很大程度上由于缺乏合适的制剂，果蝇多巴胺受体在调节中央突触传递中的作用尚未得到检验。本研究调查了多巴胺使用原代神经元培养物调节果蝇中兴奋性胆碱能突触传递的机制。全细胞记录表明，胆碱能兴奋性突触后电流（EPSC）被局部应用的多巴胺（10-500微米）下调。脊椎动物D1特异性激动剂SKF38393和6-氯-APB（10微米）模仿多巴胺介导的胆碱能突触传递抑制，具有更高的效力。相比之下，D2激动剂喹吡罗和溴隐亭没有改变胆碱能EPSC，表明多巴胺介导的胆碱能突触传递抑制是通过果蝇D1样受体的激活来实现的。微型EPSC的生物物理分析表明，通过激活D1样受体来抑制胆碱能的起源是突触前。胆碱能传递的多巴胺调节不是通过cAMP /蛋白激酶A信号传导途径介导的，因为在蛋白激酶A抑制剂H-89存在下，多巴胺能抑制胆碱能。此外，腺苷酸环化酶激活剂forskolin导致胆碱能EPSC频率增加而不是减少。最后，我们表明激活D1样受体通过抑制兴奋性胆碱能传递降低了果蝇神经元中动作电位的频率。我们所有的数据表明，果蝇神经元中D1样受体的激活会负面调节兴奋性胆碱能突触传递，从而抑制神经元的兴奋性。

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