Evaluation of long-lasting sensorimotor consequences following neonatal hypoxic-ischemic brain injury in rats: the neuroprotective role of MgSO4.

Perinatal asphyxia (PA) is a major determinant for long-term sensorimotor and locomotor deficits. The model of neonatal hypoxia-ischemia (HI) in 7-day-old rats produces sensorimotor cortex, thalamus and striatum injury, which are all critical for the maintenance of sensory motor function. The aim of this study was to evaluate the long-term neurodevelopmental disturbances in the above experimental model and to assess the neuroprotective effect of MgSO(4) in terms of long-term behavioral and morphological changes. Seven-day-old rats were separated into three groups: A (control), neither ligated nor exposed to hypoxia; B (HI/MgSO(4)) ligated, exposed to hypoxia and treated with MgSO(4) (2 g/kg b.w., i.p.), and C (HI) ligated and exposed to hypoxia. At the age of 42 days, the behavior of the rats was evaluated using 5 sensorimotor tests. Muscle power, motor coordination, reflexes, and limb placing were tested to different sensory stimuli. The study was completed with the histopathological evaluation of brain tissue damage. In all individual tests the HI-treated rats performed significantly worse than the control and MgSO(4)-treated rats and this difference was more pronounced in the limb placing tests. Additionally, neonatal HI resulted in extensive neuronal damage that was limited after MgSO(4) administration. Behavioral alterations represent a useful endpoint for studying the consequences of a perinatal HI insult and the efficacy of potential neuroprotective treatments. MgSO(4) administration resulted in prevention of HI-induced sensorimotor deficits and brain injury.