The decreased susceptibility to the development of in vitro kindling-like state in hippocampal CA1 slices of rats sensitive to audiogenic seizures.

The field excitatory postsynaptic potential (fEPSP) with the presynaptic fiber volley (PrV) and the population spike (PS) were recorded with two glass microelectrodes in stratum radiatum and stratum pyramidale of rat hippocampal CA1 slices, respectively, in response to electric stimulation of Schaffer collaterals/commissural fibers (SC/CF) containing glutamate as a neurotransmitter. Three components of the overall input-output function were taken: (1) PrV amplitude vs. intensity of stimulating current, (2) dendritic layer fEPSP slope vs. PrV amplitude and (3) PS amplitude vs. fEPSP slope. Three groups of rats were used: (1) normal male Wistar rats (control), (2) a strain of rats genetically-prone to audiogenic seizures (GPAS) and (3) GPAS rats 10 min after a single intense sound stimulus. Unlike hippocampal slices taken from normal Wistar rats, slices taken from GPAS rats were less susceptible to the development of the in vitro kindling-like state induced by the repeated 30 s applications (3 episodes) of [K+]o up to 20 mM. Such short-term [K+]o increases also did not induce the EPSP-spike transfer potentiation (E-S potentiation) in CA1 pyramidal neurons of audiogenic rats either. Furthermore, the presynaptic glutamatergic fibers of GPAS rats are less excitable to stimulating currents then that of normal Wistar rats. It is suggested that the resistance of audiogenic rat hippocampal CAI slices to the development of long lasting epileptiform activity is a protective adaptive mechanism preventing the propagation of seizure activity into limbic structures.