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首页> 外文期刊>The European Journal of Neuroscience >Localization and function of pre- and postsynaptic kainate receptors in the rat globus pallidus.
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Localization and function of pre- and postsynaptic kainate receptors in the rat globus pallidus.

机译：突触前和突触后海藻酸盐受体在大鼠苍白球的定位和功能。

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Kainate receptors (KARs) are widely expressed the basal ganglia. In this study, we used electron microscopic immunocytochemistry and whole-cell recording techniques to examine the localization and function of KARs in the rat globus pallidus (GP). Dendrites were the most common immunoreactive elements, while terminals forming symmetric or asymmetric synapses and unmyelinated axons comprised most of the presynaptic labeling. To determine whether synaptically released glutamate activates KARs, we recorded excitatory postsynaptic currents (EPSCs) in the GP following single-pulse stimulation of the internal capsule. 4-(8-Methyl-9H-1,3-dioxolo[4,5 h]{2,3}benzodiazepine-5-yl)-benzenamine hydrochloride (GYKI 52466, 100 microm), an alpha-amino-3-hydroxyl-5-methyl-4-isoxazole propionic acid (AMPA) receptor antagonist, reduced but did not completely block evoked EPSCs. The remaining EPSC component was mediated through activation of KARs because it was abolished by 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX), an AMPA/KAR antagonist. The rise time (10-90%) and decay time constant (tau) for those EPSCs were longer than those of AMPA-mediated EPSCs recorded before GYKI 52466 application. KAR activation inhibited EPSCs. This inhibition was associated with a significant increase in paired-pulse facilitation ratio, suggesting a presynaptic action of KAR. KAR inhibition of EPSCs was blocked by the G-protein inhibitor, N-ethylmaleimide (NEM), or the protein kinase C (PKC) inhibitor calphostin C. Our results demonstrate that KAR activation has dual effects on glutamatergic transmission in the rat GP: (1) it mediates small-amplitude EPSCs; and (2) it reduces glutamatergic synaptic transmission through a presynaptic G-protein coupled, PKC-dependent, metabotropic mechanism. These findings provide evidence for the multifarious functions of KARs in regulating synaptic transmission, and open up the possibility for the development of pharmacotherapies to reduce the hyperactive subthalamofugal projection in Parkinson's disease.
机译：海藻酸盐受体（KARs）广泛表达基底神经节。在这项研究中，我们使用电子显微镜免疫细胞化学和全细胞记录技术来检查大鼠苍白球（GP）中KAR的定位和功能。树突是最常见的免疫反应元件，而形成对称或不对称突触和未髓鞘轴突的末端构成了突触前标记的大部分。为了确定突触释放的谷氨酸是否激活KAR，我们在单脉冲刺激内囊后在GP中记录了兴奋性突触后电流（EPSC）。 4-（8-甲基-9H-1,3-二氧戊环[4,5 h] {2,3}苯二氮杂-5-基）-苯甲胺盐酸盐（GYKI 52466，100微米），α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体拮抗剂可减少但不能完全阻断诱发的EPSC。剩余的EPSC成分是通过激活KAR介导的，因为它被AMPA / KAR拮抗剂6-氰基-7-硝基喹喔啉-2，3-二酮（CNQX）消除了。这些EPSC的上升时间（10-90％）和衰减时间常数（tau）比使用GYKI 52466之前记录的AMPA介导的EPSC长。 KAR激活抑制了EPSC。这种抑制与配对脉冲促进比率的显着增加有关，表明KAR的突触前作用。 KAR对EPSC的抑制被G蛋白抑制剂，N-乙基马来酰亚胺（NEM）或蛋白激酶C（PKC）抑制剂钙磷蛋白C阻断。我们的结果表明，KAR活化对大鼠GP中的谷氨酸能传递具有双重影响： 1）调解小幅度EPSC; （2）它通过突触前G蛋白偶联，PKC依赖性，代谢型机制减少谷氨酸能突触传递。这些发现为KAR在调节突触传递中的多种功能提供了证据，并为开发药物疗法以减少帕金森氏病中丘脑下丘脑过度活跃的可能性开辟了可能性。

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