首页> 外文期刊>Journal of Neural Transmission >Kainate receptor-mediated presynaptic inhibition converges with presynaptic inhibition mediated by Group II mGluRs and long-term depression at the hippocampal mossy fiber-CA3 synapse
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Kainate receptor-mediated presynaptic inhibition converges with presynaptic inhibition mediated by Group II mGluRs and long-term depression at the hippocampal mossy fiber-CA3 synapse

机译:海藻酸酯受体介导的突触前抑制与II型mGluRs介导的突触前抑制和海马苔藓纤维CA3突触的长期抑制融合

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摘要

Kainate receptors (KARs) effect depression of glutamate release at hippocampal mossy fiber-CA3 (MF-CA3) synapses by a metabotropic action involving adenylyl cyclase (AC) inhibition, cAMP reduction, and diminished protein kinase A (PKA) activation. Using hippocampal slices, we show here that KAR activation interferes with the depression of glutamate release produced by Group II metabotropic glutamate receptor stimulation and low frequency stimulation (LFS)-induced long-term depression (LTD), also expressed through presynaptic AC/cAMP/PKA at MF-CA3 synapses. The mutual occlusion of depression mediated by presynaptic KARs, Group II mGluR and LFS-induced LTD suggests their mechanistic convergence at the MF-CA3 synapse and thus invokes KARs in synaptic plasticity manifest in LTD.
机译:海藻酸盐受体(KARs)通过涉及腺苷酸环化酶(AC)抑制,cAMP减少和蛋白激酶A(PKA)激活减弱的代谢作用,抑制海马苔藓纤维CA3(MF-CA3)突触中谷氨酸的释放。使用海马切片,我们在这里显示KAR激活会干扰由II组代谢型谷氨酸受体刺激和低频刺激(LFS)引起的长期抑郁症(LTD)产生的谷氨酸释放抑制,这也通过突触前AC / cAMP / MF-CA3突触处的PKA。由突触前KAR,II组mGluR和LFS诱导的LTD介导的抑郁症的相互闭塞表明它们在MF-CA3突触中的机制趋同,从而在LTD的突触可塑性中表现出KAR。

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