ABSTRACT
Background and Purpose: Despite widespread research on epilepsy, the mechanism of its insidnece is still unknown. Since the activity of ATPase plays a vital role in changing ATP into AMP, and this substance can later turn into adenosine which is the most important endogenous anticonvulsant agent in brain, the effect of inhibition of ATPase on perforant path kindling was investigated in the present study
Methods and Materials: In this experimental study, animals were kindled by electrical stimulations of the perforant path [12 times a day with a frequency of 50 Hz and pulse duration of 1 millisecond]. Upon kindling, behavioral and electrophysiologic measures of convulsions and filed potentials were recorded. For investigating the role of ATPase in animal groups, FPL 67156 was injected as the inhibitor of the ATPase after kindling stimulations ended each day. Kindled animals were 6, and there were 4 rats in other groups. Repeated measures ANOVA and Bonferoni test were used to compare the statistical quantities of fEPSP and PS of epilepsy creation in different groups of the study. Comparing the difference of paired pulses between groups was conducted by Bonferoni test. The five-stage convulsion of the groups was compared through Kruskall Wallis and Mann Whitney U tests. Statistical analyses were conducted in Prism 5
Results: The results indicated that ATPase inhibition [by injecting FPL 67156] causes no change in various behavioral stages of convulsion and daily afterdischarge duration following kindling [P>0.05]; however, it affects synapsis formation, so that PS increases in comparison with the kindled group [P<0.05] and inceases the lowering of paired pulses [P<0.05]
Conclusion: The results indicated that the activity of ATPase plays an inhibitory role on the formation in bringing about epiliepsy by kindling, so that by controlling it, it is facilitated
ABSTRACT
Adenosine is an endogenous anticonvulsant which exerts its anticonvulsant effects through adenosine Al receptors. As the piriform/amygdala is a critical circuit for limbic seizure propagation, in this study the role of amygdala Al receptors on piriform cortex kindled seizures was investigated. Rats were kindled by daily electrical stimulation of piriform cortex. In the first experiment fully kindled animals received intra-amygdala N6-cyclohexyladenosine [CHA; 10-500 micro M, a selective Al receptor] or 2% lidocaine [for reversal neuronal inhibition] bilaterally. 5 min later, animals were stimulated and seizure parameters were measured. In the second experiment, the effect of daily microinjection of CHA [100 microM] into the amygdala on piriform cortex kindling rate was investigated. Different doses of CHA had no effect on kindled seizure parameters. On the other hand, intra-amygdala 2% lidocaine reduced the kindled seizures severity. There were significant increase in stage 4 latency and decrease in stage 5 duration. Also, daily intra-amygdala CHA had no significant effect on kindling rate. The amygdala neuronal activity has a role in propagation of epileptic seizures from piriform cortex. Elimination of this activity by lidocaine decreases the severity of piriform cortex kindled seizures. However, the amygdala Al receptors have no role in this regard