Abstract
In the central nervous system, synaptic strength is regulated partly by changes in the function and number of postsynaptic glutamate receptors. The NMDA (N-methyl-D-aspartate) subtype of glutamate receptor (NMDAR) is regulated in part by the opposing actions of protein tyrosine kinases and phosphotyrosine phosphatases. Members of the Src family of protein tyrosine kinases upregulate NMDAR function, thereby gating the production of NMDAR-dependent synaptic potentiation. Src family kinases (SFKs) are a crucial point of convergence for signalling pathways that enhance NMDAR activity, so that SFKs act as a molecular hub for the control of NMDARs. These kinases regulate synaptic strength and are therefore vital for processes that underlie physiological and pathological plasticity in the brain and spinal cord.
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