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首页> 外文期刊>Neuron >Group 1 mGluR-dependent synaptic long-term depression: mechanisms and implications for circuitry and disease.
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Group 1 mGluR-dependent synaptic long-term depression: mechanisms and implications for circuitry and disease.

机译:第1组mGluR依赖性突触长期抑制:机制及对电路和疾病的影响。

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摘要

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.
机译:许多兴奋性突触在突触后密度的外围表达第1组或Gq偶联的代谢型谷氨酸受体(Gp1 mGluRs)。 Gp1 mGluRs的激活通常会响应强活性而发生,并在许多大脑区域(包括新皮质,海马,中脑,纹状体和小脑)触发突触传递的长期可塑性。在这里,我们专注于mGluR引起的长期突触性抑郁(LTD),并回顾涉及Gp1 mGluRs在行为,学习和记忆的可塑性方面的文献。此外,最近研究mGluR-LTD分子机制的研究发现与智力低下,自闭症,阿尔茨海默氏病,帕金森氏病和药物成瘾有关。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提供对脑疾病的认识。

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