Kindling Session Research Articles

Enhancement of recurrent inhibition by angular bundle kindling is retained in hippocampal slices.

Rats were kindled in the right angular bundle. EEG and monosynaptically evoked responses were monitored in the ipsilateral fascia dentata. Although every animal was kindled, Long Term Potentiation (LTP) of monosynaptic responses was observed only in part of the kindling sessions, suggesting that LTP is not required for kindling. Paired pulse inhibition of granule cell discharge was progressively enhanced by kindling. Transverse hippocampal slices (400-700 micron) of fully kindled rats were prepared 1 hour after the last seizure. Field potentials evoked by stimulation appeared completely normal. Spontaneous epileptiform discharges were not observed in control solution, in low [Ca++]0, in high [K+]0 or after high frequency stimulation. Paired pulse inhibition was enhanced in fascia dentata, but not in area CA1. Enhancement of inhibition may be caused by increased activity of inhibitory synapses or by a nonsynaptic hyperpolarizing current. The relation between the absence of spontaneous activity and enhanced inhibition in the fascia dentata is unclear.

Effect of locus ceruleus stimulation on the development of kindled seizures

The effects of locus ceruleus stimulation on amygdala kindling development were investigated. Twenty to thirty minutes of locus ceruleus stimulation was delivered prior to each amygdala kindling session. Locus ceruleus-stimulated animals spent a significantly longer time in stage 1 than did nonstimulated or reticular formation stimulated controls. However, the total number of stimulations to produce the first stage 5 did not differ between groups. The afterdischarge duration in locus ceruleus-stimulated animals increased even though the behavioral stages did not progress. There appeared to be an uncoupling of the electrographic and behavioral manifestations of the kindling process in the locus ceruleus-stimulated animals. These data support the view of an inhibitory role of the central noradrenergic system in the development of kindled seizures.