IMBALANCE IN HIPPOCAMPAL NETWORK SYNCHRONY DURING EPILEPTOGENESIS
Abstract number :
IW.03
Submission category :
13. Neuropathology of Epilepsy
Year :
2008
Submission ID :
8388
Source :
www.aesnet.org
Presentation date :
12/5/2008 12:00:00 AM
Published date :
Dec 4, 2008, 06:00 AM
Authors :
Sachin Talathi, D. Hwang, W. Ditto, Alex Cadotte and Paul Carney
Rationale: Neuronal circuitry within the hippocampus show a marked plasticity associated with the epileptic seizures. The question remains whether the observed changes in the hippocampal network are the consequence of or the cause for spontaneous epileptic seizures. One solution to resolve this dilemma is to look for a macroscopic indicator of the rewiring within the hippocampal neuronal circuitry during epileptogenesis. Methods: Experiments were performed on four 2-month old male Sprague Dawley rats. Neural signals were obtained using 16 microwire electrodes implanted bilaterally in the hippocampal CA1 and dentate gyrus subfields. Two rats were electrically stimulated until sustained electrographical and behavioral seizures were observed. Subsequently rats were monitored with continuous video-EEG and were screened for the occurrence of their first spontaneous seizure. High amplitude population spikes corresponding to the field activity of the inhibitory and excitatory postsynaptic potentials (fEPSPs and fIPSPs respectively) were extracted. The set of population spikes from the 32 recorded channels were clustered into 8 groups representing the data recorded from the four bilateral hippocampal sub-fields: the left CA1 (LCA), the left dentate gyrus (LDG), the right CA1 (RCA) and the right dentate gyrus (RDG). A simple measure of synchrony, “Event Synchronization” (ES)that determines the fraction of spike pair events matching in time was extracted. Results: Pairwise ES estimates of the instantaneous synchrony between the fEPSPs and the fIPSPs recorded from the hippocampal CA1 and dentate gyrus subfields were obtained for two time intervals (sham-control and latent periods). Surrogate analysis was used to determine the statistical significance of the true ES estimate. Time epochs when the true estimate of ES did not differ from the estimate of ES from surrogate data (<2σ) were eliminated and the amplitude variation in ES estimate of synchrony over the two time periods was determined through a least-squares straight line fit with function of form ES(t)=Dt+c (0≦t≦1). In the Figure 1 and 2 below we show the mean rate of positive/negative drift (D<0/D>
Neuropathology of Epilepsy