Gαq-deficient mice lack metabotropic glutamate receptor-dependent long-term depression but show normal long-term potentiation in the hippocampal CA1 region
Gαq-deficient mice lack metabotropic glutamate receptor-dependent long-term depression but show normal long-term potentiation in the hippocampal CA1 region
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DOI：
10.1523/jneurosci.21-14-04943.2001
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发表时间：
2001-07-15
影响因子：
5.3
通讯作者：
Offermanns, S
中科院分区：
文献类型：
--
作者：
Kleppisch, T;Voigt, V;Offermanns, S
长时程增强（LTP）和抑制（LTD）是参与学习和记忆的潜在细胞机制。I组代谢型谷氨酸受体（mGluR），与G（q）家族的异源三聚体G蛋白（G（q）和G（11））相连，已被报道促进海马LTP和LTD。为了评估它们在突触可塑性中的功能作用，我们研究了野生型、G α（q）（-/-）、和G α（11）（-/-）小鼠。在G α（q）、（-/-）和G α（11）（-/-）小鼠中，突触传递的基本参数没有改变。此外，这些小鼠对强破伤风和弱破伤风的反应显示正常的LTP。然而，在G α（q）（-/-）小鼠中不存在由I组mGluRs激动剂或由成对脉冲低频刺激（PP-LFS）诱导的LTD。此外，PP-LFS在这些小鼠中引起突触传递的增强，其不受NMDAR拮抗剂AP-5的影响。这些结果表明，G（q）在mGluR依赖性LTD中起着至关重要的作用，而海马LTP不受G（q）家族单个成员缺失的影响。
Long-term potentiation (LTP) and depression (LTD) are potential cellular mechanisms involved in learning and memory. Group I metabotropic glutamate receptors (mGluR), which are linked to heterotrimeric G-proteins of the G(q) family (G(q) and G(11)), have been reported to facilitate both hippocampal LTP and LTD. To evaluate their functional role in synaptic plasticity, we studied LTD and LTP in the CA1 region of the hippocampus from wild-type, G alpha (q)(-/-), and G alpha (11)(-/-) mice. Basic parameters of the synaptic transmission were not altered in G alpha (q),(-/-) and G alpha (11)(-/-) mice. Moreover, these mice showed normal LTP in response to a strong tetanus and to a weak tetanus. However, LTD induced either by a group I mGluRs agonist or by paired-pulse low-frequency stimulation (PP-LFS) was absent in G alpha (q)(-/-) mice. Moreover, PP-LFS caused potentiation of the synaptic transmission in these mice that was not affected by the NMDAR antagonist AP-5. These results show that G(q) plays a crucial role in the mGluR-dependent LTD, whereas hippocampal LTP is not affected by the lack of a single member of the G(q) family.