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

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 s...

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Bibliographic Details
Published in:The Journal of neuroscience 2013-05, Vol.33 (19), p.8483-8493
Main Authors: Wen, Jing A, DeBlois, Mark C, Barth, Alison L
Format: Article
Language:English
Subjects:
Afferent Pathways - physiology
Anesthetics, Local - pharmacology
Animals
Animals, Newborn
Biophysics
Central Nervous System Stimulants - pharmacology
Electric Stimulation
Excitatory Amino Acid Antagonists - pharmacology
Excitatory Postsynaptic Potentials - drug effects
Excitatory Postsynaptic Potentials - physiology
Green Fluorescent Proteins - genetics
In Vitro Techniques
Membrane Potentials - physiology
Mice
Mice, Inbred C57BL
Mice, Transgenic
Neocortex - cytology
Neocortex - growth & development
Neuronal Plasticity - physiology
Neurons - physiology
Patch-Clamp Techniques
Picrotoxin - pharmacology
Sensory Deprivation - physiology
Tetrodotoxin - pharmacology
Time Factors
Vibrissae - innervation
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Summary: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.
ISSN:0270-6474
1529-2401
1529-2401
DOI:10.1523/JNEUROSCI.3575-12.2013