Arancibia-Cárcamo I. Lorena, Fairfax Benjamin P., Moss Stephen J., Kittler Josef T.
Alterations in the activity of post-synaptic neurotransmitter receptors including α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors, N-methyl-D-aspartate (NMDA) receptors, kainate receptors and gamma hydroxybutric acid type A (GABA) receptors make an important contribution to modulation of synapse strength, neuronal excitability and the plasticity of synapses. Changes in the strength of neurotransmitter receptor signalling are thought to be achieved, in part, by the modulation of channel gating and conductance or by regulating the number or location of receptors expressed on cell surface and synaptic membranes. Neurotransmitter receptor trafficking is now recognized as a key mechanism for altering the strength of synapses during synaptic plasticity by changing synaptic receptor number [1]. Here, we focus on receptor membrane trafficking and, in particular, receptor endocytosis as a mechanism to regulate the number of surface and synaptic neurotransmitter receptors. We briefly review some general cellular mechanisms that underlie surface membrane protein internalization and then discuss in detail some of the cell biological approaches that have been important for studies of neurotransmitter receptor trafficking.
突触后神经递质受体活性的改变,包括α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体、N-甲基-D-天冬氨酸(NMDA)受体、海人藻酸受体和γ-氨基丁酸A型(GABA)受体,对突触强度、神经元兴奋性和突触可塑性的调节起着重要作用。神经递质受体信号强度的变化被认为部分是通过调节通道门控和电导,或通过调节细胞表面和突触膜上表达的受体数量或位置来实现的。神经递质受体运输现在被认为是通过改变突触受体数量来改变突触可塑性期间突触强度的关键机制[1]。在这里,我们关注受体膜运输,特别是受体内吞作用,作为调节表面和突触神经递质受体数量的一种机制。我们简要回顾一些表面膜蛋白内化所依据的一般细胞机制,然后详细讨论一些对神经递质受体运输研究很重要的细胞生物学方法。