Group 1 mGluR-dependent synaptic long-term depression: mechanisms and implications for circuitry and disease.

Group 1 mGluR-dependent synaptic long-term depression: mechanisms and implications for circuitry and disease.
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DOI:
10.1016/j.neuron.2010.01.016
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发表时间:
2010-02-25
期刊:
影响因子:
16.2
通讯作者:
Huber KM
Huber KM
中科院分区:
医学1区
文献类型:
--
作者:
Lüscher C;Huber KM

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许多兴奋性突触在突触后密度的外围表达第1组或GQ偶联的代谢性谷氨酸受体(Gp1 MGluRs)。Gp1 mGluRs的激活通常发生在对强烈活动的反应中,并在许多大脑区域触发突触传递的长期可塑性,包括新皮质、海马体、中脑、纹状体和小脑。在这里,我们主要关注mGluR诱导的长期突触抑制(LTD),并回顾了Gp1 mGluRs在行为、学习和记忆可塑性中的作用的文献。此外,最近对mGluR-Ltd分子机制的研究发现,mGluR-Ltd与智力低下、自闭症、阿尔茨海默病、帕金森病和药物成瘾有关。我们讨论了mGluRs如何导致神经回路的可塑性,以及对mGluR可塑性的分子机制的理解如何为大脑疾病提供洞察。
Many excitatory synapses express Group 1, or Gq coupled, metabotropic glutamate receptors (Gp1 mGluRs) at the periphery of their postsynaptic density. Activation of Gp1 mGluRs typically occurs in response to strong activity and triggers long-term plasticity of synaptic transmission in many brain regions including the neocortex, hippocampus, midbrain, striatum and cerebellum. Here we focus on mGluR-induced long-term synaptic depression (LTD) and review the literature that implicates Gp1 mGluRs in the plasticity of behavior, learning and memory. Moreover, recent studies investigating the molecular mechanisms of mGluR-LTD have discovered links to mental retardation, autism, Alzheimer’s disease, Parkinson’s disease and drug addiction. We discuss how mGluRs lead to plasticity of neural circuits and how the understanding of the molecular mechanisms of mGluR plasticity provides insight into brain disease.
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