Group I mGluR Induced LTD of NMDAR-synaptic Transmission at the Schaffer Collateral but not Temperoammonic Input to CA1.
Group I mGluR Induced LTD of NMDAR-synaptic Transmission at the Schaffer Collateral but not Temperoammonic Input to CA1.
复制标题
DOI：
10.2174/1570159x13666150615221502
复制
发表时间：
2016
影响因子：
5.3
通讯作者：
Farrow P
中科院分区：
文献类型：
--
作者：
Fitzjohn S;Bashir Z;Farrow P
NMDA 受体由多个亚基组成，对于诱导突触可塑性以及学习和记忆至关重要。在本研究中，应用 I 组 mGlu 受体激动剂 DHPG 引起 Schaffer 侧支 NMDA-EPSC (DHPG-LTDNMDA) 的长期限制，但不会导致海马 CA1 神经元上的颞氨途径 NMDA-EPSC 的长期限制。 DHPG-LTDNMDA 不会改变 NMDA-EPSC 对 GluN2B 拮抗剂 Ro25-6981 的敏感性，表明 DHPG-LTDNMDA 后突触后 NMDA 受体亚基组成保持不变。此外，GluN2B 受体的阻断不影响 DHPG-LTDNMDA 的诱导。这些结果表明，同一 CA1 神经元上的两个突触之间的 NMDA 受体可塑性存在差异，但表明 NMDA 受体的亚基组成并不能解释这种差异。
NMDA receptors are composed of multiple subunits and are crucial in the induction of synaptic plasticity and learning and memory. In this study, application of the group I mGlu receptor agonist, DHPG, caused LTD of NMDA-EPSCs (DHPG-LTDNMDA) of the Schaffer collateral, but not of NMDA-EPSCs of the temperoammonic pathway onto CA1 neurons of the hippocampus. DHPG-LTDNMDA did not alter the sensitivity of NMDA-EPSC to the GluN2B-antagonist, Ro25-6981, indicating that the postsynaptic NMDA receptor subunit composition remained unchanged following DHPG-LTDNMDA. Furthermore, blockade of GluN2B receptors did not affect the induction of DHPG-LTDNMDA. These results demonstrate a difference in the plasticity of NMDA receptors between two synapses onto the same CA1 neuron, but indicate that the subunit composition of NMDA receptors does not account for this difference.