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首页> 外文期刊>The European Journal of Neuroscience >Synaptic release of dopamine in the subthalamic nucleus.
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Synaptic release of dopamine in the subthalamic nucleus.

机译：丘脑底核中多巴胺的突触释放。

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Abstract The direct modulation of subthalamic nucleus (STN) neurons by dopamine (DA) neurons of the substantia nigra (SN) is controversial owing to the thick caliber and low density of DA axons in the STN. The abnormal activity of the STN in Parkinson's disease (PD), which is central to the appearance of symptoms, is therefore thought to result from the loss of DA in the striatum. We carried out three experiments in rats to explore the function of DA in the STN: (i) light and electron microscopic analysis of tyrosine hydroxylase (TH)-, dopamine beta-hydroxylase (DbetaH)- and DA-immunoreactive structures to determine whether DA axons form synapses; (ii) fast-scan cyclic voltammetry (FCV) to determine whether DA axons release DA; and (iii) patch clamp recording to determine whether DA, at a concentration similar to that detected by FCV, can modulate activity and synaptic transmission/integration. TH- and DA-immunoreactive axons mostly formed symmetric synapses. Because DbetaH-immunoreactive axons were rare and formed asymmetric synapses, they comprised the minority of TH-immunoreactive synapses. Voltammetry demonstrated that DA release was sufficient for the activation of receptors and abolished by blockade of voltage-dependent Na(+) channels or removal of extracellular Ca(2+). The lifetime and concentration of extracellular DA was increased by blockade of the DA transporter. Dopamine application depolarized STN neurons, increased their frequency of activity and reduced the impact of gamma-aminobutyric acid (GABA)-ergic inputs. These findings suggest that SN DA neurons directly modulate the activity of STN neurons and their loss may contribute to the abnormal activity of STN neurons in PD.
机译：摘要黑质（SN）的多巴胺（DA）神经元直接调节丘脑下核（STN）神经元的原因是STN口径厚而密度低。因此，STN在帕金森氏病（PD）中的异常活动是症状出现的关键，因此被认为是纹状体中DA的丧失所致。我们在大鼠中进行了三个实验，以探讨DA在STN中的功能：（i）酪氨酸羟化酶（TH）-，多巴胺β-羟化酶（DbetaH）-和DA免疫反应性结构的光电子显微镜分析，以确定DA是否轴突形成突触; （ii）快速扫描循环伏安法（FCV），以确定DA轴突是否释放DA; （iii）膜片钳记录以确定DA（其浓度与FCV检测的浓度相似）是否可​​以调节活性和突触传递/整合。 TH和DA免疫反应性轴突大多形成对称突触。由于DbetaH免疫反应性轴突很少见，并形成不对称突触，因此它们占TH免疫反应性突触的少数。伏安法表明DA释放足以激活受体，并被电压依赖性Na（+）通道的阻断或细胞外Ca（2+）的清除所取消。阻断DA转运蛋白可延长细胞外DA的寿命和浓度。多巴胺的应用使STN神经元去极化，增加了它们的活动频率，并减少了γ-氨基丁酸（GABA）能量输入的影响。这些发现表明SN DA神经元直接调节STN神经元的活性，其丢失可能导致PD中STN神经元的异常活性。

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