The initiation and spread of epileptiform bursts in the in vitro hippocampal slice.
We recorded spontaneous synchronized epileptiform bursts from hippocampal slices from guinea pig using an array of 16 extracellular electrodes placed over the stratum pyramidale of CA2 and CA3. The slices were made epileptogenic with the GABA antagonist picrotoxin (or occasionally penicillin). We found that spontaneous bursts always originate at a discrete focus at or near CA2. These bursts spread smoothly and uniformly across CA3 at an average velocity of 0.13 m/s. This velocity is slower than the conduction velocity of the Schaffer collaterals or mossy fibers. Picrotoxin produced afterdischarges following the initial primary burst, and these afterdischarges were found to originate and spread in a fashion nearly identical to the primary burst. These results indicate that CA2 is a unique region which must possess unusual cellular and/or synaptic connectivity properties which result in a decreased threshold for initiation of epileptiform activity. We consider several hypothetical patterns of local synaptic connectivity in the light of these results, and we discuss the possible role of residual inhibition in limiting the spread of synchronized discharges.
D000818:Animals; D004594:Electrophysiology; D004827:Epilepsy / Q000139:chemically induced / Q000503:physiopathology*; D006168:Guinea Pigs; D006624:Hippocampus / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009431:Neural Conduction; D009433:Neural Inhibition; D010406:Penicillins; D010852:Picrotoxin; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission
D010406:Penicillins; D010852:Picrotoxin