Can lateralizing sensorimotor deficits be identified after neonatal cerebral hypoxia-ischemia in rats?

The neonatal rat model of unilateral cerebral hypoxia-ischemia (HI) is commonly used to test the efficacy of therapeutic strategies for prevention or treatment of stroke in the immature brain. Traditionally neuroprotection has been defined as reduction in tissue injury; there is growing interest in complementary functional assessment. Our objectives were to determine whether lateralizing performance deficits could be detected in two sensorimotor tests not previously used after neonatal HI, and to determine whether performance reflected the extent of tissue damage. Seven-day-old rats that underwent right carotid ligation followed by 1.5 h in 8% O2 and age-matched controls were tested for sensorimotor performance on postnatal day 35 (P35). We evaluated initial forepaw placement on the wall of a cylinder, and time taken to contact and remove adhesive stickers from the dorsum of each forepaw. Cortical, striatal and hippocampal damage severity was evaluated on P36 by calculating the contralateral-ipsilateral percent difference in regional areas. There was an inverse relationship between cortical and striatal damage severity and percent contralateral forepaw initiation in the cylinder. There was a direct linear relationship between damage severity and the delay from contact to removal of the contralateral sticker. These two tests revealed quantifiable contralateral sensorimotor deficits 4 weeks after unilateral neonatal cerebral HI in animals with cortical and striatal damage.