We tested the hypothesis that basal ganglia (BG) structures show selective neuronal vulnerability and that AMPA receptor blockade protects cells within the glutamatergic corticostriatal pathways after asphyxie cardiac arrest in oneweek-old piglets. Anesthetized piglets were exposed to 30 rain of hypoxia followed by 7 min of airway occlusion. NBQX (n=10) or vehicle (n=10) was administered before airway occlusion (30 mg/kg, i.v.) and during the first 4 h of recovery (IS mg/kg/h). Four piglets in each group died in status epilepticus (usually at 24-48 h). Neuronal survival at 96 h was highly topographic in location. Number of viable neurons in caudate (C) was significantly higher than in putamen (P) (59±28 vs. 33±25; ±SD, p<0.001) or in substantia nigra pars reticulau (SNr) (<1%). Neuronal survival was not improved by NBQX in C (S7±24) or P (20±1756) compared to vehicle in C (62±33%) or P (46±32 ). Survival in P and SNr was less man in primary sensorimotor cortex with NBQX (45±28X) or vehicle (78±13%). When groups were pooled, occurrence of non-lethal seizure activity reduced neuronal survival in C (49±27 vs. 80±12%) and P (18±17 vs. 63±21%;p<0.02). We conclude that postatphyxic basal ganglia damage is highly selective in neonatal pigs and is distributed via cortical-subcortical pathways. Seizure activity worsened histopathology, possibly by excitotoxic corticostriatal activation, and AMPA receptor blockade failed to protect against neuronal damage within this pathway. (Supported by NS20020).
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology