Voltage depth profiles of high-frequency oscillations after kainic acid-induced status epilepticus.
High-frequency oscillations (HFOs) have been described in normal and epileptic brains of animals and humans. These oscillations reflect a short-term integration within neuronal networks and have important functional consequences for normal and pathological processes. We performed a comparative voltage depth profile analysis of normal and pathological HFOs after intrahippocampal kainic acid injection. Sixteen channel recording probes, with 100-200 microm separation between the tips of microelectrodes, were implanted along the CA1-dentate gyrus axis in the anterior hippocampus of adult rats. Guide cannulae were implanted in the CA3 area. After a week of baseline recording kainic acid (KA) (0.2microg/0.2microl) was injected into the CA3 area. Electrical activity continued to be record for the next 3-4 weeks after KA induced status epilepticus. Voltage depth profiles and power spectral analysis of HFOs were performed off-line using DataPac software. Ripple oscillations (80-200 Hz) in the CA1 area and gamma activity (40-80 Hz) in the dentate gyrus remained after status epilepticus. In the group of rats that later developed seizures a new pattern consisting of bursts of population spikes (BPS) occurred. The maximum of amplitude for BPS generated in CA1 was in the pyramidal layer and for those generated in the dentate gyrus was in the granular layer. BPS appeared 2-3 days after status epilepticus and remained for the rest of the experiments. The frequencies of intraburst spikes varied between 80 Hz and 600 Hz. With increasing distance from the area of the burst generation, this activity took on the appearance of HFOs. The occurrence of spontaneous BPS appear to be a primary electrophysiological consequence of status epilepticus when progressive epileptogenesis occurs with maximum of amplitude in the cellular layer. In areas outside of the generator of the BPS, this activity looks more like pathological high-frequency oscillations (pHFO), which were observed in earlier experiments.
Bragin
Anatol
A
Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA. abragin@ucla.edu
Wilson
Charles L
CL
Engel
Jerome
J
D000818:Animals; D018891:Dentate Gyrus / Q000187:drug effects / Q000503:physiopathology; D004567:Electrodes, Implanted; D004569:Electroencephalography / Q000706:statistics & numerical data*; D004594:Electrophysiology; D005071:Evoked Potentials / Q000187:drug effects; D006624:Hippocampus / Q000503:physiopathology*; D007608:Kainic Acid / Q000494:pharmacology; D017966:Pyramidal Cells / Q000187:drug effects / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013226:Status Epilepticus / Q000139:chemically induced* / Q000503:physiopathology*
D007608:Kainic Acid