Initiation, labile, and stabilization phases of experience-dependent plasticity at neocortical synapses.

Citation data:

The Journal of neuroscience : the official journal of the Society for Neuroscience, ISSN: 1529-2401, Vol: 33, Issue: 19, Page: 8483-93

Publication Year:
2013
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Citations 11
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Repository URL:
http://repository.cmu.edu/biology/3
PMID:
23658185
DOI:
10.1523/jneurosci.3575-12.2013
PMCID:
PMC3740338
Author(s):
Wen, Jing A.; DeBlois, Mark C.; Barth, Alison L.
Publisher(s):
Society for Neuroscience
Tags:
Neuroscience; Afferent Pathways; Anesthetics; Local; Animals; Newborn; Biophysics; Central Nervous System Stimulants; Electric Stimulation; Excitatory Amino Acid Antagonists; Excitatory Postsynaptic Potentials; Green Fluorescent Proteins; Membrane Potentials; Mice; Inbred C57BL; Transgenic; Neocortex; Neuronal Plasticity; Neurons; Patch-Clamp Techniques; Picrotoxin; Sensory Deprivation; Tetrodotoxin; Time Factors; Vibrissae; Biology
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article description
Alteration of sensory input can change the strength of neocortical synapses. Selective activation of a subset of whiskers is sufficient to potentiate layer 4-layer 2/3 excitatory synapses in the mouse somatosensory (barrel) cortex, a process that is NMDAR dependent. By analyzing the time course of sensory-induced synaptic change, we have identified three distinct phases for synaptic strengthening in vivo. After an early, NMDAR-dependent phase where selective whisker activation is rapidly translated into increased synaptic strength, we identify a second phase where this potentiation is profoundly reduced by an input-specific, NMDAR-dependent depression. This labile phase is transient, lasting only a few hours, and may require ongoing sensory input for synaptic weakening. Residual synaptic strength is maintained in a third phase, the stabilization phase, which requires mGluR5 signaling. Identification of these three phases will facilitate a molecular dissection of the pathways that regulate synaptic lability and stabilization, and suggest potential approaches to modulate learning.