The Network And Cellular Electrophysiological Mechanisms Of Cortical Or Hippocampal Epilepsy Induced By Tatenization Of The Right Dosal Hippocampus In Rats

The purpose of the present work was to study hippocampal cellular electrophysiological mechanisms of cortical or hippocampal epilepsy reorganized by acute tetanization (60 Hz, 2 s, 0.4-0.6 mA) of the right posterior dorsal hippocampus (ATPDH). Experiments were performed on 35 adult male Sprague-Dawley rats to establish epilepsy model. Four-channel recordings were simultaneously done, two channels for single unit recordings from bilateral hippocampal CAl areas and another two channels for electrocorticogram (ECoG) recordings from the surface of neocortex or hippocampal electroencephalogram (EEG) recordings from CAl areas on bilateral sides. The ATPDH induced that: (1) Epileptic ECoG activities originated from single unit afterdischarges of the ipsilateral hippocampal neuron, followed by single unit afterdischarges of the contralateral hippocampal neuron, finally 10Hz ECoG seizure-like oscillations appeared bilaterally. Furthermore, rhythmic 4-10Hz ECoG oscillations were bilaterally enhanced. (2) Hippocampal EEG fast oscillations were bilaterally evoked, while the bilateral hippocampal neurons fired asymmetrically. (3) The hippocampal neuronal firing interspike interval (ISI) spots distributed in an irregular circular shape. It was more regular on the ipsilateral side. (4) On the contralateral side both ECoG wave interpeak interval (IPI) and hippocampal neuronal firing ISI spot distributed in a " ム "-shaped. (5) Maximum peaks of hippocampal EEG rhythmic oscillations fluctuated in regular sinusoidal pattern and time-locked to the circular ISI spot distribution of hippocampal neuronal firing. The results indicate that bilateral epileptic hippocampal-neocortical networks might be reorganized by the ATPDH. During epileptic network reorganization, the hippocampal neuronal firing encodes temporally its information in particular irregular circular shape ISI distribution, which correlated with hippocampal or cortical network seizures. It implies the network and cellular electrophysiological mechanisms and its possible coding properties of ATPDH-induced cortical and hippocampal epilepsy.