Quantitative analysis of contralateral hemisphere hypertrophy and sensorimotor performance in adult rats following unilateral neonatal ischemic-hypoxic brain injury.
The immature nervous system is capable of considerable compensatory reorganization following injury. This has been studied extensively following many different types of injury in humans and laboratory animals. One common risk factor associated with perinatal brain injury that has been associated with such reorganization is an ischemic-hypoxic event. Using the established Levine model of neonatal ischemic-hypoxia (IH) to create unilateral striatal, cortical and hippocampal damage, we investigated anatomical changes in the undamaged hemisphere contralateral to the injury. Specifically, we measured cross-sectional area (mm2) of brain sections at the level of +1.20 and -2.12 mm from bregma. In addition, we examined sensorimotor deficits in these animals during development and as adults by measuring the amount of time that the animals were able to remain on a rotating treadmill. Our results show that some animals exhibited hypertrophy in the hemisphere contralateral to the lesion as compared to measurements taken from normal control animals. Additionally, we have demonstrated that, following IH, animals that showed significant contralateral whole-hemisphere hypertrophy were able to remain on the Rota-Rod treadmill significantly longer than the animals that did not exhibit this hypertrophy. We conclude that there are compensatory reorganizational changes that occur in the undamaged hemisphere contralateral to injury in some animals following neonatal ischemic-hypoxic brain injury. Furthermore, our data suggest that this plasticity in the contralateral hemisphere may be functionally advantageous.
Jansen
E M
EM
Department of Neurosurgery, University of Minnesota Medical School, Minneapolis 55455, USA.
Low
W C
WC
D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D007839:Functional Laterality; D006984:Hypertrophy; D002534:Hypoxia, Brain / Q000473:pathology / Q000503:physiopathology*; D002546:Ischemic Attack, Transient / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009043:Motor Activity; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values