Postsynaptic control of plasticity in developing somatosensory cortex

THE rearrangement of synaptic connections during normal and deprived development is thought to be controlled by correlations in afferent impulse activity1. A favoured model is based on postsynaptic detection of synchronously active afferents; synapses are stabilized when pre- and postsynaptic activity is correlated and weakened or eliminated when their activity is uncorrelated2,3. Most evidence for this model comes from demonstrations that correlated afferent input is necessary for the segregation of eye-dominant inputs in the developing vertebrate visual system1,4,5 and that critical period plasticity of ocular dominance columns in cat visual cortex is disrupted by blockade of postsynaptic transmission6–8. We tested whether the developmental plasticity of somatosensory columns, known as 'barrels', in rodent primary somatosensory cortex (S1)9–13 is similar to that of ocular dominance columns. We report here that the selective disruption of postsynaptic activation in rat S1 by application of a glutamate receptor antagonist inhibits rearrangements in the somatotopic patterning of thalamocorticalafferents induced by manipulations of the sensory periphery during the critical period. These findings show that postsynaptic activation has a prominent role in critical period plasticity in S1 cortex.

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