Abstract
The neuronal dendritic tree is a key determinant of how neurons receive, compute, and transmit information. During early postnatal life, synaptic activity promotes dendrite elaboration. Spinal motor neurons utilize GluA1-containing AMPA (2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl) propanoic acid) receptors (AMPA-R) to control this process. This form of developmental dendrite growth can occur independently of N-methyl-d-aspartate receptors (NMDA-R). This review focuses on the mechanism by which the GluA1 subunit of AMPA-R transforms synaptic activity into dendrite growth, and describes the essential role of the GluA1 binding partner SAP97 (synapse-associated protein of 97 kDa molecular weight) in this process. This work defines a new mechanism of activity-dependent development, which might be harnessed to stimulate the recovery of function following insult to the central nervous system.