Cortical Plasticity and Behavioral Recovery Following Focal Lesion to Primary Motor Cortex in Adult Rats

Acquired brain injuries, such as ischemic stroke and traumatic brain injury, are the leading causes of physical disabilities. Previously, scientists have shown that damage of the primary motor cortex induced neural plasticity in the premotor area in human and non-human primate studies. Neural plasticity, particularly within the same hemisphere of the lesion (ipsilesional), is thought to contribute to and account for functional recovery. It is not yet known to what extent plasticity mediates recovery and how to take advantage of neural plasticity to maximize the functional outcome. Rodent models are most often used not only for studying the role of motor cortex in motor skill learning but also in neurodegenerative research. To further elucidate the role of adaptive plasticity in the ipsilesional hemisphere during the recovery of upper limb function, we aimed to establish the baseline neural changes after a focal cortical injury. Therefore, we took advantage of two separate cortical motor areas, in the Rattus norvegicus, from which the corticospinal tracts terminate in the motor nuclei of the cervical level spinal cord, controlling upper extremity musculature--the first, a more caudally located subregion of M1, often referred to as the caudal forelimb area (CFA), and the second, a more rostrally located non-primary area, referred to as the rostral forelimb area (RFA). The objective of this dissertation work was to characterize physiological changes in RFA during the complex and lengthy process of recovery using rat models of focal cortical trauma and cortical ischemia restricted to CFA. The results demonstrated that the post-injury cortical plasticity in RFA may play a role in functional recovery. Further, we showed differential effects of rehabilitative training on ipsilesional RFA plasticity after CFA ischemic injury. Extensive physiological changes were evident past rehabilitative training. Thus, neural plasticity in RFA appeared to be dependent both on post-lesion motor experience and time. The dissertation work supports the hypothesis that cortical plasticity within the spared RFA after restrictive damage to CFA mediates use-dependent physiological reorganization, which provides a substrate for sustaining rehabilitation-aided motor functional recovery