Martenson James S, Tomita Susumu
Program in Cellular Neuroscience, Neurodegeneration and Repair (CNNR), Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510, USA.
Program in Cellular Neuroscience, Neurodegeneration and Repair (CNNR), Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510, USA.
Curr Opin Pharmacol. 2015 Feb;20:102-8. doi: 10.1016/j.coph.2014.11.011. Epub 2014 Dec 17.
Ionotropic neurotransmitter receptors mediate fast synaptic transmission by localizing at postsynapses. Changes in receptor number at synapses induce synaptic plasticity. Thus, mechanisms for the synaptic localization of receptors in basal transmission and synaptic plasticity have been investigated extensively. Recent findings reveal that synaptic localization of tetrameric AMPA receptors in basal transmission requires the PDZ binding of TARP auxiliary subunits, which modulate receptor properties and pharmacology. On the other hand, pentameric GABAA receptors require multiple receptor subunits for their synaptic localization in basal transmission. AMPA receptors seem to utilize distinct mechanisms for basal synaptic localization and synaptic insertion during plasticity. Revealing precise mechanisms for receptor synaptic localization may establish new approaches to control synaptic transmission.
离子型神经递质受体通过定位于突触后部位来介导快速突触传递。突触处受体数量的变化会诱导突触可塑性。因此，人们对受体在基础传递和突触可塑性过程中的突触定位机制进行了广泛研究。最近的研究结果表明，在基础传递中，四聚体AMPA受体的突触定位需要TARP辅助亚基的PDZ结合，TARP辅助亚基可调节受体特性和药理学特性。另一方面，五聚体GABAA受体在基础传递中的突触定位需要多个受体亚基。AMPA受体在基础突触定位和可塑性过程中的突触插入似乎利用了不同的机制。揭示受体突触定位的精确机制可能会建立控制突触传递的新方法。
