The role of
inflammation has been shown in the pathogenesis of
epilepsy, while
glucocorticoids and
adrenaline have anti-inflammatory effects. The aim of the present study was to investigate the effects of
adrenaline,
prednisolone, and
indomethacin on
caffeine-induced
epilepsy (epileptiform activity) in rats and to examine the mechanism of the pro-epileptic effect of
indomethacin. The adrenalectomized rats that had been given only
adrenaline (the control group) did not die; however,
adrenaline did not prevent the adrenalectomized rats which were given
prazosin,
phenoxybenzamine,
yohimbine,
metoprolol, and
propranolol from dying. In the rats given
propranolol +
adrenaline, the rate of death was 100%, while this rate was 50% in the groups receiving
prazosin +
adrenaline,
phenoxybenzamine +
adrenaline, and
metoprolol +
adrenaline. The rate was 75% in the group given
yohimbine +
adrenaline.
Prednisolone increased the degree of convulsion in adrenalectomized rats. Over-reduction in the blood
catecholamine level made epileptogenesis more severe. It was observed that
adrenaline pressed epileptogenesis via its own receptors (α - 1, α - 2, β - 1, β - 2). It was also revealed that all of the
adrenergic receptors were responsible due to
antiepileptic activity; β - 2 receptors played the most important role. It was observed that both acute and chronic
indomethacin administration reduced the
catecholamine levels. The situation in which acute administration of
indomethacin did not affect epileptogenesis might originate from the fact that the structure of
indomethacin did not significantly increase the
corticosterone level.