Abstract
Cerebral palsy (CP) is a group of movement and posture disorders attributed to insults in the developing brain. In rats, CP-like motor deficits can be induced by early hind-limb sensorimotor restriction (SR; from postnatal days P2 to P28), associated or otherwise with perinatal anoxia (PA; on P0 and P1). In this study, we address the question of whether PA, early SR or a combination of both produces alterations to sensorimotor development. Developmental milestones (surface righting, cliff aversion, stability on an inclined surface, proprioceptive placing, auditory startle, eye opening) were assessed daily from P3 to P14. Motor skills (horizontal ladder and beam walking) were evaluated weekly (from P31 to P52). In addition, on P52, the thickness of the somatosensory (S1) and cerebellar cortices, and corpus callosum were measured, and the neuronal and glial cell numbers in S1 were counted. SR (with or without PA) significantly delayed the stability on an inclined surface and hastened the appearance of the placing reflex and impaired motor skills. No significant differences were found in the thickness measurements between the groups. Quantitative histology of S1 showed that PA, either alone or associated with SR, increased the number of glial cells, while SR alone reduced neuronal cell numbers. Finally, the combination of PA and SR increased the size of neuronal somata. We conclude that SR impairs the achievement of developmental milestones and motor skills. Moreover, both SR and PA induce histological alterations in the S1 cortex, which may contribute to sensorimotor deficits.
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