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首页> 外文期刊>Journal of Neurophysiology >Metabotropic glutamate receptor-mediated presynaptic depression at corticostriatal synapses involves mGLuR2 or 3.
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Metabotropic glutamate receptor-mediated presynaptic depression at corticostriatal synapses involves mGLuR2 or 3.

机译：皮质口突触的代谢型谷氨酸受体介导的突触前抑制涉及mGLuR2或3。

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摘要

1. The pharmacology of the metabotropic glutamate receptor (mGluR) that mediates synaptic depression at corticostriatal synapses was investigated with the use of field potential and whole cell patch-clamp recording from striatal slices and whole cell recordings from isolated striatal neurons. 2. The mGluR2,3-selective agonists (R,S)-4-carboxy-3-hydroxyphenylglycine (CHPG), (2S, 1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl) glycine (DCG-IV), and (2S, 3S, 4S)-alpha-(carboxycyclopropyl) glycine (L-CCG-I) inhibited the synaptically driven population spike (PS) evoked by afferent stimulation during field potential recording in striatal slices. These agonists also inhibited excitatory postsynaptic potentials (EPSPs) evoked by afferent stimulation during whole cell recordings. The metabotropic receptor antagonist R,S-alpha-methyl-4-carboxyphenylglycine (MCPG) blocked the synaptic depressant actions of DCG-IV and trans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD). 3. The mGluR4,6,7-selective agonist L-serine-O-phosphate (L-SOP) did not alter corticostriatal synaptic transmission, but both this agonist and the mGluR4,6,7 agonist D,L-2-amino-4-phosphonobutyric acid (AP4) reduced the amplitude of the population EPSP and PS evoked in the dentate gyrus (DG) by stimulation of the lateral perforant path (LPP). These data are consistent with earlier observations that AP4 does not inhibit corticostriatal transmission, but produces presynaptic depression at LPP-DG synapses. 4. Application of mGluR agonists that inhibited transmission did not alter the input resistance or excitability of striatal neurons and did not inhibit responses evoked by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor activation.(ABSTRACT TRUNCATED AT 250 WORDS)
机译：1.利用场电位和纹状体切片的全细胞膜片钳记录以及离体纹状体神经元的全细胞记录，研究了介导皮质口突触突触抑制的代谢型谷氨酸受体（mGluR）的药理学。 2. mGluR2,3-选择性激动剂（R，S）-4-羧基-3-羟苯基甘氨酸（CHPG），（2S，1'R，2'R，3'R）-2-（2,3-二羧基环丙基）甘氨酸（DCG-IV）和（2S，3S，4S）-α-（羧基环丙基）甘氨酸（L-CCG-1）抑制纹状体切片在场电势记录过程中传入刺激引起的突触驱动的种群峰值（PS） 。这些激动剂还抑制了全细胞记录过程中传入刺激引起的兴奋性突触后电位（EPSPs）。促代谢受体拮抗剂R，S-α-甲基-4-羧基苯基甘氨酸（MCPG）阻断了DCG-IV和反-1-氨基环戊烷-1,3-二羧酸（t-ACPD）的突触抑制作用。 3. mGluR4,6,7选择性激动剂L-丝氨酸-O-磷酸（L-SOP）不会改变皮层皮质突触传递，但该激动剂和mGluR4,6,7激动剂D，L-2-氨基- 4-膦基丁酸（AP4）通过刺激侧向穿孔路径（LPP）降低了齿状回（DG）中诱发的种群EPSP和PS的振幅。这些数据与较早的观察结果一致，即AP4不会抑制皮层皮质的传递，但会在LPP-DG突触处产生突触前抑制。 4.抑制传递的mGluR激动剂的应用不会改变纹状体神经元的输入阻力或兴奋性，也不会抑制由α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）/海藻酸酯受体激活引起的反应（摘要以250字截断）

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