Cellular Electrophysiological Mechanism Of Epileptic Networks In Dual Hippocampi Reestablished By Tetanization Of The Right Caudate Putamen In Rats

The purpose was to study the cellular electrophisiological mechanism of epileptic networks in dual hippocampi reestablished by overactivation of the right caudate putamen (CPu). The experiments were performed on 101 male Sprague Dawley rats weighting 200~250g. Acute tetanization (60Hz, 2s, 0.4~0.6mA) of the right caudate putamen (ATRC) or of the right dorsal hippocampus (ATRDH) was administrated to establish rat epilepsy model. A pair of single unit recordings from bilateral hippocampi was simultaneously used to detect the effects of the ATRC or those of the ATRDH, bilateral hippocampal depth electrograhgh were also simultaneously recorded after the ATRC. Neuronal epilepsy-related firing patterns were analyzed according to activated neural pathway length from the RCPu to the dual hippocampi, or from the right dorsal HPC to ipsilateral hippocampal local networks and contralateral HPC. Results demonstrated that: (1) ATRC could facilitate the formation of hippocampal epileptic networks, and presented the synchronaztion of epilepsy related electric activities in bilateral hippcampi. (2) The firing pattern of single hippocampal neuron was obviously modulated both by the ATRC and by the ATPDH. There were long duration bursting (650.738?6.419 ms, n=120) with short interbursting interval (IBI)(772.600 +46.665ms, n=90) of single neuron induced by the ATRC, while short duration bursting (270.612 + 19.917 ms, n=123) (T=6.353, P<0.001)of single neuron with long IBI(1373.663 ?121.236ms, n=103) (T=4.627, P<0.001)by the ATPDH. (3) There were long duration single unit afterdischarges (7.06 +0.776s, n=104) with long latency (8.77 + 1.231trains, n=30) induced by the ATRC, while short duration single unit afterdischarges(3.93 + 0.657S, n=33)( T=0.3079, P<0.001)with short latency (3.33+ 0.681trains, n=15) (7=3.681, P0.001) induced by the ATPDH. (4) ATRC could induce the immediate transition between single unit bursting and afterdischarges. (5) Pairs of cellular electric activities in bilateral hippocampi were synchronouse or interactive inhibiting after repeated administration of the ATRC. The results suggest that long duration single unit bursting or afterdischarges in bilateral hippocampi could be brought about by overactivation oflong-distance neural pathway from the right CPu to the dual hippocampi, which might be an important cellular mechanism of hippocampal epileptic networks reconstruction. From these phenomina the following conclusion can be drawn that there was different information encoding charisteristic when different neural pathway was activated. The activated CPu-HPC functional neural pathway might act as the amplifier of the signal of epilepsy-related activities of single neuron in bilateral hippocampi.