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代谢型谷氨酸受体对齿状回门区边界中间神经元突触输入的差异性调节

Differential regulation of synaptic inputs to dentate hilar border interneurons by metabotropic glutamate receptors.

作者信息

Doherty J, Dingledine R

机构信息

Department of Pharmacology, Emory University Medical School, Atlanta, Georgia 30322, USA.

出版信息

J Neurophysiol. 1998 Jun;79(6):2903-10. doi: 10.1152/jn.1998.79.6.2903.

DOI:10.1152/jn.1998.79.6.2903
PMID:9636096
Abstract

Regulation of synaptic transmission by metabotropic glutamate receptors (mGluRs) was examined at two excitatory inputs to interneurons with cell bodies at the granule cell-hilus border in hippocampal slices taken from neonatal rats. Subgroup-selective mGluR agonists altered the reliability, or probability of transmitter release, of evoked minimal excitatory synaptic inputs and decreased the amplitudes of excitatory postsynaptic currents (EPSCs) evoked with conventional stimulation. The group II-selective agonist, (2S,1R',2R',3R')-2-(2, 3-dicarboxylcyclopropyl) glycine (DCG-IV; 1 microM), reversibly depressed the reliability of EPSCs evoked by stimulation of the dentate granule cell layer. However, DCG-IV had no significant effect on EPSCs evoked by CA3 stimulation in the majority (82%) of hilar border interneurons. Both the group III-selective agonist, -(+)-2-amino-4-phosphonobutyric acid (-AP4; 3 microM), and the group I-selective agonist, (RS)-3,5-dihydroxyphenylglycine (DHPG; 20 microM) reversibly depressed synaptic input to interneurons from both CA3 and the granule cell layer. We conclude that multiple pharmacologically distinct mGluRs presynaptically regulate synaptic transmission at two excitatory inputs to hilar border interneurons. Further, the degree of mGluR-meditated depression of excitatory drive is greater at synapses from dentate granule cells onto interneurons than at synapses from CA3 pyramidal cells.

摘要

在取自新生大鼠的海马切片中,对位于颗粒细胞-海马回边界处的中间神经元的两个兴奋性输入进行了代谢型谷氨酸受体(mGluRs)对突触传递调节的研究。亚型选择性mGluR激动剂改变了诱发的最小兴奋性突触输入的可靠性或递质释放概率,并降低了常规刺激诱发的兴奋性突触后电流(EPSCs)的幅度。II组选择性激动剂(2S,1R',2R',3R')-2-(2,3-二羧基环丙基)甘氨酸(DCG-IV;1 microM)可逆地降低了刺激齿状颗粒细胞层诱发的EPSCs的可靠性。然而,在大多数(82%)海马回边界中间神经元中,DCG-IV对CA3刺激诱发的EPSCs没有显著影响。III组选择性激动剂-(+)-2-氨基-4-膦酰丁酸(-AP4;3 microM)和I组选择性激动剂(RS)-3,5-二羟基苯甘氨酸(DHPG;20 microM)均可逆地降低了来自CA3和颗粒细胞层的中间神经元的突触输入。我们得出结论,多种药理学上不同的mGluRs在突触前调节海马回边界中间神经元的两个兴奋性输入处的突触传递。此外,mGluR介导的兴奋性驱动抑制程度在齿状颗粒细胞到中间神经元的突触处比在CA3锥体细胞的突触处更大。

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