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首页> 外文期刊>The European Journal of Neuroscience >Midbrain muscarinic receptor mechanisms underlying regulation of mesoaccumbens and nigrostriatal dopaminergic transmission in the rat.
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Midbrain muscarinic receptor mechanisms underlying regulation of mesoaccumbens and nigrostriatal dopaminergic transmission in the rat.

机译：中脑毒蕈碱受体机制在大鼠中介导的蓄积调节和黑纹状体多巴胺能传递。

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Abstract Laterodorsal (LDT) and pedunculopontine (PPT) tegmental nuclei in the mesopontine project cholinergic inputs to the midbrain ventral tegmental area (VTA) and substantia nigra pars compacta (SNc), respectively, to directly and indirectly influence the activity of dopamine neuronal cells via actions on muscarinic and nicotinic receptors. The present study investigated the role of midbrain muscarinic receptors in the functional modulation of VTA and SNc dopamine cell activity as reflected by alterations in, respectively, nucleus accumbens (NAc) and striataldopamine efflux. In vivo chronoamperometry was used to measure changes in basal dopamine efflux via stearate-graphite paste electrodes implanted unilaterally in the NAc or striatum of urethane-anaesthetized rats, following blockade or activation of, respectively, VTA or SNc muscarinic receptors. Intra-VTA or -SNc infusion of the muscarinic antagonist scopolamine (200 microg/microL) reduced, respectively, NAc and striatal dopamine efflux while infusion of the muscarinic and nicotinic agonist carbachol (0.5 microg/microL) or the prototypical muscarinic agonist muscarine (0.5 microg/microL) increased NAc and striatal dopamine efflux. Transient decreases in dopamine efflux preceded these increases selectively in the striatum, suggesting a reduction in excitatory or increase in inhibitory drive to the SNc by preferential activation of M3 muscarinic receptors on GABA interneurons and glutamatergic inputs. This was confirmed by showing that selective blockade of M3 receptors with p-F-HHSiD (0.5 microg/microL) increased striatal, but not NAc, dopamine efflux. Together, these findings suggest that midbrain muscarinic receptors, probably M5 subtypes on VTA and SNc dopamine neurons, contribute to the tonic excitatory regulation of forebrain basal dopamine transmission whereas presynaptic M3 receptors serve to counter excessive excitation of nigral dopamine cell activity.
机译：摘要中脑桥脑区的背外侧核（LDT）和足小脑桥墩（PPT）的被膜核向中脑腹侧被膜区（VTA）和黑质致密部（SNc）分别提供胆碱能输入，以直接或间接影响多巴胺神经元细胞的活动对毒蕈碱和烟碱样受体的作用。本研究调查中脑毒蕈碱受体在VTA和SNc多巴胺细胞活性的功能性调节中的作用，分别通过伏伏核（NAc）和纹状体多巴胺外排的改变反映出来。体内计时电流法用于分别阻断或激活VTA或SNc毒蕈碱受体后，通过单侧植入氨基甲酸乙酯麻醉的大鼠的NAc或纹状体中的硬脂酸盐-石墨糊状电极测量基础多巴胺流出量的变化。毒蕈碱拮抗剂东pol碱（200 microg / microL）的VTA或-SNc输注分别降低了NAc和纹状体多巴胺外排，同时注入毒蕈碱和烟碱激动剂卡巴胆碱（0.5 microg / microL）或典型的毒蕈碱激动剂毒蕈碱（0.5） microg / microL）增加NAc和纹状体多巴胺外排。多巴胺外排的短暂减少先于这些纹状体的增加，这表明通过优先激活GABA中神经元上的M3毒蕈碱受体和谷氨酸能输入，兴奋性降低或对SNc的抑制性驱动增加。通过显示用p-F-HHSiD（0.5 microg / microL）选择性阻断M3受体，可以增加纹状体的多巴胺流出，而不是NAc的多巴胺流出。总之，这些发现表明，中脑毒蕈碱受体（可能是VTA和SNc多巴胺神经元上的M5亚型）有助于前脑基底多巴胺传递的兴奋性兴奋性调节，而突触前M3受体则用于抵消黑质多巴胺细胞活性的过度兴奋。

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