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首页> 外文期刊>The European Journal of Neuroscience >Distinct properties of presynaptic group II and III metabotropic glutamate receptor-mediated inhibition of perforant pathway-CA1 EPSCs.
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Distinct properties of presynaptic group II and III metabotropic glutamate receptor-mediated inhibition of perforant pathway-CA1 EPSCs.

机译：突触前组II和III代谢型谷氨酸受体介导的穿孔途径CA1 EPSC的抑制特性。

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Abstract I have compared the effects of group II or III metabotropic glutamate receptor (mGluR) activation on monosynaptic excitatory responses recorded intracellularly from CA1 pyramidal neurons of rat hippocampus and evoked by perforant pathway stimulation in vitro. The excitatory postsynaptic currents (EPSCs) were reduced either by the group II mGluR agonist LY354740 (500 nm, 31 +/- 6% of control) or by the group III agonist L-AP4 (400 micro m, 53 +/- 5% of control). Both drugs enhanced EPSC paired-pulse facilitation (range 125-189% of control). These effects were blocked by the broad-spectrum mGluR antagonist LY341495 (1 or 20 micro m) which when applied alone did not significantly change the EPSCs elicited at low (0.1-0.2 Hz) or higher (1-100 Hz) frequency of stimulation. Prior reduction of the EPSCs induced by L-AP4 did not occlude the subsequent inhibition elicited by LY354740. The effect of LY354740, but not that of L-AP4, was blocked in the presence of the cAMP analogue Sp-cAMPS (20 micro m) and with the K(+) channel antagonist alpha-dendrotoxin (125 nm). In contrast, the effect of L-AP4, but not that of LY354740, was prevented by the calmodulin inhibitor ophiobolin A (25 micro m) and with the N-type Ca(2+) channel antagonist omega-conotoxin-GVIA (1 micro m). In the presence of the P/Q type Ca(2+) channel antagonist omega-agatoxin-IVA (400 nm), the EPSCs were depressed either by LY354740 or by L-AP4. Groups II and III mGluRs are segregated at the presynaptic terminal, and there are distinct differences between the properties of the presynaptic inhibition mediated by these two groups of receptors.
机译：摘要我比较了II型或III型代谢型谷氨酸受体（mGluR）激活对大鼠海马CA1锥体神经元细胞内记录的单突触兴奋性反应的影响，并在体外通过穿孔途径刺激引起了这种作用。 II组mGluR激动剂LY354740（500 nm，对照的31 +/- 6％）或III组激动剂L-AP4（400 microm，53 +/- 5％）降低了兴奋性突触后电流（EPSC）控制）。两种药物均能增强EPSC配对脉冲的促成作用（控制范围的125-189％）。这些作用被广谱mGluR拮抗剂LY341495（1或20微米）所阻断，当单独使用时，它不会显着改变在低（0.1-0.2 Hz）或更高（1-100 Hz）刺激频率下引起的EPSC。由L-AP4诱导的EPSC的先前减少不排除LY354740引起的随后的抑制。在存在cAMP类似物Sp-cAMPS（20微米）的情况下，并用K（+）通道拮抗剂α-树突毒素（125 nm）阻断LY354740的作用，而不是L-AP4的作用。相比之下，钙调蛋白抑制剂ophiobolin A（25微米）和N型Ca（2+）通道拮抗剂ω-芋螺毒素-GVIA（1微米）阻止了L-AP4的作用，但没有阻止LY354740的作用m）。在P / Q型Ca（2+）通道拮抗剂Ω-agatoxin-IVA（400 nm）的存在下，LY354740或L-AP4抑制了EPSCs。第II组和第III组mGluR在突触前末端隔离，并且这两类受体介导的突触前抑制特性之间存在明显差异。

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