J Neurophysiol (April 1, 2003). 10.1152/jn.01053.2002
Submitted on Submitted 21 November 2002; accepted in final form 3 December 2002

Developmental Regulation of Plasticity in the Forepaw Representation of Ferret Somatosensory Cortex

Department of Anatomy and Cell Biology and Program in Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814

McLaughlin, Debra F. and Sharon L. Juliano. Developmental Regulation of Plasticity in the Forepaw Representation of Ferret Somatosensory Cortex. J. Neurophysiol. 89: 2289-2298, 2003. This study characterized the spatiotemporal responses in ferret somatosensory cortex after sensory deprivation at different phases of cortical development. We hypothesized that cortical responses to stimulation of intact superficial radial nerve in adults will vary systematically according to maturation of thalamocortical relationships at the time of an ulnar nerve transection. Depending on the age of the animal at the time of the lesion, we found differential effects on the spatial distribution of the short- and long-latency components of the cortical response. In animals lesioned at postnatal days 5-7, when thalamic projections are not yet stabilized and layer 4 is not yet formed, we found that initial (short-latency) cortical responses are widespread and fragmented. Ulnar nerve transections performed at postnatal day 20 or 21, when thalamocortical afferents are more stabilized and layer 4 is clearly identifiable, yield moderate expansions in the distribution of short- and long-latency components of the cortical response. Nerve lesions in adults lead to a wider distribution of long-latency cortical activity. Neonatal lesions broaden the spatial distribution and increase the latency of the initial cortical response; interruption of nerve input in older juveniles alters both the early and later components; and nerve lesions in adult animals expand the distribution of later cortical activity only. These findings demonstrate correlation between developmental phase at the time sensory input is interrupted and the latency of affected components of the cortical response. This supports the hypothesis that differential response changes are regulated by functional reorganization of thalamocortical connections after neonatal lesions and alteration of corticocortical dynamics after adult lesions.