Effect of quinolinic acid administered during pregnancy on the brain of offspring.

The brains of rat offspring were histologically and histochemically examined after quinolinic acid administration to mothers during the gestation period. Quinolinic acid was administered intraperitoneally in a dose of 30 or 60 mmol, once daily, throughout the entire gestation period. Brain specimens were taken on days 1, 5, and 21 after birth from experimental and control animals. The neuronal cell body injury was detected in the selected brain formations. More profound alterations were seen in the substantia nigra and cerebral cortex, especially within the entorhinal area, whereas much less damage was noted in the striatum and hippocampus. Strongly pronounced symptoms of cerebral edema were seen. Histochemically, an increased activity of NADPH-reductase within neuronal cell bodies of the pyramidal layer in the hippocampus, striatum and cerebral cortex was demonstrated. The decrease of activity of succinic and alpha-glycerophosphate dehydrogenases within areas of tissue spongiosis was noted. The weak overall activity of MAO made it impossible to register changes in its intensity. No changes in the Ca-ATP-ase activity in brain formations after quinolinic acid treatment were observed. It has been reported that excitotoxic brain injury caused by quinolinic acid displays a selective pattern of neuronal degeneration that affects neuronal cell bodies but spares axons at the site of intracerebral injections (Schwarcz et al. 1983; Lehmann et al. 1985; Vezzani et al. 1986), as well as following systemic administration (Beskid and Markiewicz 1988; Beskid and Finiewicz-Murawiejska 1992). The excitotoxic activity of this compound can be detected by making use of the properties of the N-methyl-D-aspartate (NMDA) receptor agonist (Stone et al. 1987).(ABSTRACT TRUNCATED AT 250 WORDS)