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海人藻酸受体介导的突触前抑制与II型代谢型谷氨酸受体介导的突触前抑制以及海马苔藓纤维-CA3突触处的长时程抑制汇聚。

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.

作者信息

Negrete-Díaz J V, Sihra T S, Delgado-García J M, Rodríguez-Moreno A

机构信息

División de Neurociencias, Universidad Pablo de Olavide, Seville, Spain.

出版信息

J Neural Transm (Vienna). 2007;114(11):1425-31. doi: 10.1007/s00702-007-0750-4. Epub 2007 May 18.

DOI:10.1007/s00702-007-0750-4
PMID:17510730
Abstract

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.

摘要

海人藻酸受体（KARs）通过一种涉及抑制腺苷酸环化酶（AC）、降低环磷酸腺苷（cAMP）以及减少蛋白激酶A（PKA）激活的代谢型作用，抑制海马苔藓纤维 - CA3（MF - CA3）突触处谷氨酸的释放。利用海马脑片，我们在此表明，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）诱导的长时程抑制（LTD）所产生的谷氨酸释放抑制，后者同样通过MF - CA3突触处的突触前AC/cAMP/PKA来表达。由突触前KARs、II组代谢型谷氨酸受体（mGluR）和LFS诱导的LTD介导的抑制作用相互重叠，这表明它们在MF - CA3突触处的机制趋同，从而使KARs参与到LTD所表现出的突触可塑性中。

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2
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Proc Natl Acad Sci U S A. 2006 Apr 18;103(16):6380-5. doi: 10.1073/pnas.0601267103. Epub 2006 Apr 10.
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Long-term depression of kainate receptor-mediated synaptic transmission.
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