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首页> 外文期刊>The European Journal of Neuroscience >Dopamine action in the substantia nigra pars reticulata: iontophoretic studies in awake, unrestrained rats.
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Dopamine action in the substantia nigra pars reticulata: iontophoretic studies in awake, unrestrained rats.

机译：多巴胺在黑质网中的作用：在清醒，不受约束的大鼠中进行离子电渗疗法研究。

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摘要

Dopamine (DA) neurons located in the substantia nigra pars compacta release DA not only via axonal terminals, affecting neurotransmission within the striatum, but also via dendrites, some of which densely protrude into the substantia nigra pars reticulata (SNr). Although the interaction of dendritically released DA with somatodendritic autoreceptors regulates DA cell activity, released DA may also affect SNr neurons. These cells, however, lack postsynaptic DA receptors, making it unclear how locally released DA modulates their activity. Although previous work in brain slices suggests that DA might modulate the activity of GABA inputs, thus affecting SNr neurons indirectly, it remains unclear how increased or decreased DA release might affect these cells exposed to normal afferent inputs. To explore this issue, we examined the effects of iontophoretic DA and amphetamine on SNr neurons in awake, unrestrained rats. DA had no consistent effects on SNr cells but amphetamine, known to induce DA release, dose-dependently inhibited most of them. This effect was blocked by SCH23390, a selective D1 receptor blocker, which itself strongly increased neuronal discharge rate. As GABA input is a major factor regulating the activity of SNr neurons, our data suggest that dendritically released DA, by interacting with D1 receptors on striato-nigral and pallido-nigral afferents, is able to decrease this input, thus releasing SNr neurons from tonic, GABA-mediated inhibition. Surprisingly, a full DA receptor blockade (SCH23390 + eticlopride) did not result in the expected increase in SNr discharge rate, suggesting that other mechanisms are responsible for behavioral abnormalities following acute disruption of DA transmission.
机译：位于黑质致密部的多巴胺（DA）神经元不仅通过轴突末端释放DA，影响纹状体内的神经传递，还通过树突释放，其中一些树突密集地突入黑质网状组织（SNr）。尽管通过树突状释放的DA与体树突状自身受体的相互作用调节DA细胞的活性，但释放的DA也可能影响SNr神经元。但是，这些细胞缺乏突触后DA受体，因此不清楚局部释放的DA如何调节其活性。尽管先前在脑切片中的研究表明DA可能会调节GABA输入的活性，从而间接影响SNr神经元，但尚不清楚DA释放增加或减少如何影响暴露于正常传入输入的这些细胞。为了探究这个问题，我们研究了离子电渗疗法DA和苯丙胺对清醒无拘束大鼠SNr神经元的影响。 DA对SNr细胞没有一致的作用，但是已知会诱导DA释放的苯丙胺会剂量依赖性地抑制其中的大多数。选择性的D1受体阻滞剂SCH23390阻断了这一作用，它本身就大大提高了神经元放电速率。由于GABA输入是调节SNr神经元活性的主要因素，因此我们的数据表明，通过与纹状体和苍白质-黑质传入体上的D1受体相互作用，以树状释放的DA能够减少这种输入，从而从补剂中释放SNr神经元。 ，GABA介导的抑制作用。出乎意料的是，完全的DA受体阻滞剂（SCH23390 +依替普利）并未导致SNr释放速率的预期增加，表明其他机制可能导致DA传播的急性中断后的行为异常。

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