Long-term metabolic effects of pentylenetetrazol-induced status epilepticus in the immature rat.

The present study was devoted to the long-term effects of seizures induced by pentylenetetrazol in immature rats on cerebral metabolic rates in young adult animals. Seizures were induced by repetitive intraperitoneal injections of subconvulsive doses of pentylenetetrazol either in 10- (P10) or in 21- (P21) day-old rats. The long-term metabolic effects of the seizures were studied at P60 in 54 cerebral structures by means of the [14C]deoxyglucose method. At P60, metabolic activity was decreased in 10 brain regions of rats exposed to pentylenetetrazol at P10 and in 29 structures in rats exposed to seizures at P21. Among the structures whose metabolic activity was reduced at P60 by seizures occurring either at P10 or at P21 were mainly sensory, cortical and hippocampal regions plus mammillary body, i.e. all the structures metabolically characterized as most vulnerable to pentylenetetrazol-induced status epilepticus in our previous study [Pereira de Vasconcelos A. et al. (1992) Devl Brain Res. 69, 243-259]. In the animals exposed to seizures at P21, metabolic activity was also reduced at P60 in additional sensory and cortical regions, as well as in limbic, thalamic and hypothalamic nuclei, also considered as highly sensitive to short-term pentylenetetrazol-induced seizures [Pereira de Vasconcelos A. et. al. (1992)]. Rates of glucose utilization were also reduced in a few additional areas such as the monoaminergic cell groupings. In conclusion, there are some parallels between the structures metabolically most sensitive during pentylenetetrazol-induced status epilepticus in immature rats and the long-term regional metabolic decreases recorded at P60. Our data also confirm the well-known higher sensitivity to seizures during the third postnatal week in rodents.