Cortical organization after treatment of a peripheral nerve with ricin: an evaluation of the relationship between sensory neuron death and cortical adjustments after nerve injury
- PMID: 3209747
- DOI: 10.1002/cne.902770410
Cortical organization after treatment of a peripheral nerve with ricin: an evaluation of the relationship between sensory neuron death and cortical adjustments after nerve injury
Abstract
The present study was designed to assess whether cortical changes after peripheral nerve damage are related to the degree of death of primary sensory neurons in the damaged nerve. The cytotoxin ricin was injected into the sciatic nerves of adult rats to kill primary sensory neurons with axons through the injection site. Following periods of 6-101 days, the S-I hindpaw map was evaluated with neurophysiological techniques and compared with the hindpaw maps of previously studied normal adult rats and adult rats that had undergone adult or neonatal sciatic section at a comparable level of the nerve. These comparisons allowed evaluation of cortical functional organization following different degrees of sensory neuron loss after sciatic nerve injury. There were three main results. 1) The comparison of ricin-treated and normal adult rats indicated that ricin treatment interrupted inputs from the sciatic skin territory on the hindpaw and caused a limited increase in the size of the cortical area that was activated by stimulation of hindpaw skin innervated by the remaining saphenous nerve. 2) The cortical maps of rats that had undergone adult ricin treatment (relatively large primary neuron loss) or section during adulthood (small to moderate primary neuron loss) were similar. In both groups, only the saphenous hindpaw skin was represented in cortex, and the cortical area that was activated by stimulation of the saphenous hindpaw skin had undergone a comparable limited enlargement. 3) The comparison of ricin-treated adult rats (relatively large primary neuron loss) and adult rats that had undergone neonatal section (relatively large primary neuron loss) indicated that cortical organization differed after these treatments. In particular, after ricin treatment the cortical area that was activated by stimulation of the saphenous hindpaw skin was larger than the comparable area in neonatal denervates, and the topographical progressions between the hindpaw and adjacent body representations were not as variable as after neonatal section. These findings indicate that cortical maps are altered after injection of ricin into a nerve. The similarity in cortical organization after ricin treatment (relatively large sensory neuron loss) and nerve section in adults (relatively small sensory neuron loss) and the differences in cortical organization after ricin treatment and nerve section in neonates (both relatively large sensory neuron loss) indicate cortical changes do not covary as a simple function of the degree of peripheral neuron death.
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