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 uncorrelated^2,3. 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 system^1,4,5 and that critical period plasticity of ocular dominance columns in cat visual cortex is disrupted by blockade of postsynaptic transmission^6-8. 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.