Effects of sensorimotor restriction and anoxia on gait and motor cortex organization: implications for a rodent model of cerebral palsy.
Chronic or acute perinatal asphyxia (PA) has been correlated with the subsequent development of cerebral palsy (CP), a developmental neurological disorder characterized by spasticity and motor abnormalities often associated with cognitive deficits. Despite the prevalence of CP, an animal model that mimics the lifetime hypertonic motor deficits is still not available. In the present study, the consequences of PA on motor behavior, gait and organization of the primary motor cortex were examined in rats, and compared with the behavioral and neurological consequences of early postnatal movement-restriction with or without oxygen deprivation. Rats subjected to PA had mild increases in muscular tone accompanied by subtle differences in walking patterns, paralleled by significantly altered but relatively modest disorganization of their primary motor cortices. Movement-restricted rats, suffering PA or not, had reduced body growth rate, markedly increased muscular tone at rest and with active flexion and extension around movement-restricted joints that resulted in abnormal walking patterns and in a profoundly distorted representation of the hind limbs in the primary motor cortex. Within the sensorimotor-restricted groups, non-anoxic rats presented the most abnormal pattern and the greatest cortical representational degradation. This outcome further supports the argument that PA per se may represent a substrate for subtle altered motor behaviors, and that PA alone is sufficient to alter the organization of the primary motor cortex. At the same time, they also show that early experience-dependent movements play a crucial role in shaping normal behavioral motor abilities, and can make a powerful contribution to the genesis of aberrant movement abilities.
Keck Center for Integrative Neuroscience, Coleman Laboratory and Department of Otolaryngology-Head and Neck Surgery, University of California at San Francisco, 513 Parnassus Avenue HSE-832, San Francisco, CA 94143-0732, USA. fab@phy.ucsf.edu
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D000818:Animals; D000831:Animals, Newborn; D001931:Brain Mapping; D002547:Cerebral Palsy / Q000209:etiology / Q000503:physiopathology*; D004195:Disease Models, Animal; D005684:Gait / Q000502:physiology; D000860:Hypoxia / Q000150:complications*; D007794:Lameness, Animal / Q000209:etiology; D009043:Motor Activity / Q000502:physiology; D009044:Motor Cortex / Q000502:physiology* / Q000503:physiopathology; D018482:Muscle, Skeletal / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical / Q000502:physiology*