LONG-TERM EFFECTS OF PERINATAL ASPHYXIA ON BASAL GANGLIA NEUROTRANSMITTER SYSTEMS STUDIED WITH MICRODIALYSIS IN RAT

Asphyxia was induced in pups delivered by caesarean section on pregnan t Sprague-Dawley rats. Rats within the last day of gestation were anae sthetised and hysterectomized. The uterus horns including the foetuses were placed in a water bath for various periods of time. Following as phyxia the uterus horns were opened. The pups were removed, stimulated to breathe, left to recover and given to surrogate mothers. Control a nd asphyctic pups were obtained from each mother. Rats surviving asphy ctic periods longer than 20 min at 37 degrees C showed chronic deficit s in the release of neurotransmitters monitored with microdialysis in the basal ganglia. The main change observed in 6-month-old male rats t hat underwent severe perinatal asphyxia was a marked decrease in stria tal dopamine release, monitored under basal and D-amphetamine stimulat ed conditions, as compared with control (normal- or caesarean-delivere d) rats. Striatal glutamate and aspartate levels were also decreased f ollowing asphyxia. In the substantia nigra, the main effect of asphyxi a was a decrease of both gamma-aminobutyric acid (GABA) and aspartate levels. Thus, this study provides evidence that perinatal asphyxia lea ds to chronic deficits in neurotransmission in the basal ganglia.