Cortical kindled seizures: modification by excitant and depressant drugs

The effects of several excitant-convulsants, cataleptic anesthetics, and gamma-acetylenic gamma-aminobutyric acid (GABA) were tested on seizures kindled by repetitive electrical stimulation of the motor cortex in the rat. A dose response was determined for each drug. For most of the drugs, the doses tested ranged from those causing some signs of behavioral excitation to those inducing epileptoid activity. None of the excitant-convulsants, including strychnine, physostigmine, amphetamine, bicuculline, or pentylenetetrazol, increased the afterdischarge duration (AD) or behavioral response (BR) of the partially developed (PD-KCS) or generalized fully developed (KCS) kindled cortical seizures. Whereas pentylenetetrazol had no effect on the PD-KCS, it has been previously shown to increase significantly the AD and BR of the developing or partially developed amygdaloid kindled seizures. Lidocaine, gamma-butyrolactone, gamma-acetylenic GABA, phencyclidine, and ketamine inhibited the AD of the KCS by greater than or equal to 80%. Lidocaine, phencyclidine, and ketamine decreased whereas gamma-butyrolactone and gamma-acetylenic GABA increased the AD of the PD-KCS. The ability of gamma-butyrolactone and gamma-acetylenic GABA to potentiate the PD-KCS while inhibiting the KCS presents a paradox not readily explained. Our results combined with previous reports of the effects of gamma-butyrolactone and gamma-acetylenic GABA on amygdaloid kindled seizures indicate that the KCS is more susceptible to GABAnergic and cataleptic inhibition than is the fully developed amygdaloid kindled seizures. The differences between the response of cortical kindled and that of amygdaloid kindled seizures to some of the drugs tested may indicate differences in the physiological and biochemical mechanisms involved in producing these seizures.