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Plasticity after injury to the CNS
Randolph J. Nudo, Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA,
Ines Eisner-Janowicz, Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA,
Ann M. Stowe, Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA
Animal models have been especially useful in understanding the role of neuroplasticity in recovery of sensorimotor skills after brain injury. The type of injury and the method of induction vary with the specific purposes of the experiment. Typically, injuries are of two types: those designed to mimic traumatic brain injury (TBI) and those designed to mimic cerebral ischemia (or stroke). Studies conducted in cortical sensory areas over the past several years have revealed that representational maps are alterable as a function of the integrity of their sensory inputs, and as a function of experience. Changes in two neurotransmitter systems, gammaaminobutyric acid (GABA) and glutamate, have been implicated to play a role in functional recovery. New strategies for promoting recovery that were derived from basic studies in preclinical models are being tested in clinical trials. Approaches employing neurotrophins, neuromodulators, stem cells, magnetic stimulation, and electrical stimulation are currently under development.
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