Kindling-like state in rat hippocampal CA1 slices induced by the repeated short-term extracellular K+ increases: the role of L-type Ca(2+)-channels.

The repeated 30 s applications (3-6 episodes) of K+ (up to 20 mM) induced the appearance of single electric pulse-triggered population spike bursts in the rat CA1 hippocampal slices. This kindling-like state kept for a long time after the last K(+)-application and was limited by the time of slice survival. Disconnection of CA3 region did not significantly eliminate the effect of repeated short-term [K+]o increases on the establishment and maintenance of the kindling-like state in the CA1 region. This state correlated with the increases in the efficiency of the excitatory postsynaptic potential (EPSP)-spike transfer (the excitability of CA1 pyramidal neurons) but not in the glutamatergic synaptic efficiency. The selective blocker of L-type Ca2+ channels nimodipine (10 microM) abolished the development of the kindling-like state as well as the increases in the efficiency of the EPSP-spike transfer in rat hippocampal CA1 slices. Taken together, these data indicate that the described model of kindling in vitro can be useful for a study of the role of different sites of Ca2+ entry into hippocampal neurons for the cellular mechanisms of epileptogenesis.