GluA1-homomeric AMPA receptor in synaptic plasticity and neurological diseases.

Synaptic transmission is one of the fundamental processes that all brain functions are based on. Changes in the strength of synaptic transmission among neurons are crucial for information processing in the central nervous system. The α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid subtype of ionotropic glutamate receptors (AMPARs) mediate the majority of the fast excitatory synaptic transmission in the mammalian brain. Rapid trafficking of AMPARs in and out of the postsynaptic membrane is proposed to be a major mechanism for synaptic plasticity, and learning and memory. Defects in the regulated AMPAR trafficking have been shown to be involved in the pathogenesis of certain psychiatric and neurodegenerative diseases. Studies accumulated in the past 30 years have provided a detailed molecular insight on how the trafficking of AMPARs is modulated in a subunit-specific manner. In particular, emerging evidence supports that the regulated expression and trafficking of Ca2+-permeable, GluA1-homomeric subtype of AMPARs mediates diverse types of synaptic plasticity, thereby playing critical roles in brain function and dysfunction. In this review, we will discuss the current knowledge of AMPAR subunit-specific trafficking, with a particular emphasis on the involvement of GluA1-homomeric receptor trafficking in synaptic plasticity and brain disorders. This article is part of the special Issue on 'Glutamate Receptors - AMPA receptors'.