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Glutamate receptor dysfunction and drug targets across models of autism spectrum disorders

机译：谷氨酸受体功能障碍和跨自闭症谱系统模型的药物靶标

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There is strong evidence that metabotropic and ionotropic glutamate receptors are affected in autism spectrum disorders (ASD), but there are few candidate genes indicating involvement of these receptors. This suggests that glutamate receptor dysregulation may primarily be involved in the expression of ASD, but is an uncommon etiology. Directly implicated in models of fragile-X with ASD phenotypes is metabotropic glutamate receptor type 5 (mGluR5), which appears to be an effective pharmacologic target in a number of models of ASD. The review of other ASD models demonstrates that there is also evidence of a role for kainate, NMDA, and AMPA receptors in the neuropathophysiology of ASD, though the relationship between dysfunction in those receptors and ASD-associated phenotypes is not well understood. Current models indicate a way forward to delineate the role of glutamate receptors in ASD. Further development of preclinical models focusing on glutamate receptors may provide tools to target a clinically important subset of ASD symptoms.
机译：有很大的证据表明，代谢性和离子型谷氨酸受体受到自闭症谱系紊乱（ASD）的影响，但候选基因几乎没有表明这些受体的涉及。这表明谷氨酸受体失调可以主要参与ASD的表达，但是一种罕见的病因。用ASD表型的脆X模型直接涉及代言谷氨酸受体类型5（MGLUR5），其似乎是ASD的多种模型中的有效的药理学靶标。其他ASD模型的审查表明还有证据表明Kinate，NMDA和AMPA受体在ASD的神经病理学中的作用，尽管这些受体和ASD相关表型的功能障碍之间的关系并不充分了解。目前的模型表明描除谷氨酸受体在ASD中的作用的前进方向。专注于谷氨酸受体的临床前模型的进一步发展可以提供靶向临床重要症状的临床重要症状的工具。

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