January 4, 2008
Researchers at the University of Southern California and Carnegie Mellon have published a study that has implications for synaptic metaplasticity in neocortex.
Dr. Tansu Celikel, at the University of Southern California, and Dr. Alison Barth, at Carnegie Mellon University, have published a study that has implications for how synaptic plasticity in vivo is regulated following its initial induction. N-methyl-D-aspartate receptor–dependent synaptic strengthening is the most common and best-understood form of plasticity in studies of the central nervous system in vitro, and it is likely that synaptic strengthening that occurs during the course of normal behavioral experience in vivo requires NMDA receptors. However, how NMDA receptors influence plasticity after the initiation of synaptic strengthening in vivo has not been well studied. Ongoing neural activity may strengthen synapses even if plasticity is previously expressed in a given synapse, but the mechanism of this metaplasticity is not yet understood. Because experience-dependent plasticity is cumulative over time in many behaviorally relevant contexts, understanding how synaptic plasticity is modified or enhanced after its induction is critical to our ability to understand and facilitate learning.
Roger Clem, Tansu Celikel, and Alison Barth now report that while NMDA receptor dependent expression initially mediates experience-dependent plasticity during sensory stimulation, activity of NMDA receptors shunts subsequent expression of plasticity. Blocking NMDA receptor activity, however, restores the ability of synapses to express plasticity through the activation of metabotropic glutamate receptors. These results argue against the widely accepted dogma that synaptic potentiation is saturated upon expression of plasticity and identify the receptors controlling the plasticity of the synapses.The article can be accessed at Science magazine: Clem, Celikel and Barth (2008) Ongoing in vivo experience triggers synaptic metaplasticity in the neocortex. Science, 319:101-105.