PT  - JOURNAL ARTICLE
AU  - William B. J. Cafferty
AU  - Elizabeth J. Bradbury
AU  - Malcolm Lidierth
AU  - Martyn Jones
AU  - Philip J. Duffy
AU  - Sophie Pezet
AU  - Stephen B. McMahon
TI  - Chondroitinase ABC-Mediated Plasticity of Spinal Sensory Function
AID  - 10.1523/JNEUROSCI.3877-08.2008
DP  - 2008 Nov 12
TA  - The Journal of Neuroscience
PG  - 11998--12009
VI  - 28
IP  - 46
4099  - http://www.jneurosci.org/content/28/46/11998.short
4100  - http://www.jneurosci.org/content/28/46/11998.full
SO  - J. Neurosci.2008 Nov 12; 28
AB  - Experimental therapeutics designed to enhance recovery from spinal cord injury (SCI) primarily focus on augmenting the growth of damaged axons by elevating their intrinsic growth potential and/or by nullifying the influence of inhibitory proteins present in the mature CNS. However, these strategies may also influence the wiring of intact pathways. The direct contribution of such effects to functional restoration after injury has been mooted, but as yet not been described. Here, we provide evidence to support the hypothesis that reorganization of intact spinal circuitry enhances function after SCI. Adult rats that underwent unilateral cervical spared-root lesion (rhizotomy of C5, C6, C8, and T1, sparing C7) exhibited profound sensory deficits for 4 weeks after injury. Delivery of a focal intraspinal injection of the chondroitin sulfate proteoglycan-degrading enzyme chondroitinase ABC (ChABC) was sufficient to restore sensory function after lesion. In vivo electrophysiological recordings confirm that behavioral recovery observed in ChABC-treated rats was consequent on reorganization of intact C7 primary afferent terminals and not regeneration of rhizotomized afferents back into the spinal cord within adjacent segments. These data confirm that intact spinal circuits have a profound influence on functional restoration after SCI. Furthermore, comprehensive understanding of these targets may lead to therapeutic interventions that can be spatially tailored to specific circuitry, thereby reducing unwanted maladaptive axon growth of distal pathways.