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J Neurophysiol 82: 2262-2270, 1999;
0022-3077/99 $5.00
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The Journal of Neurophysiology Vol. 82 No. 5 November 1999, pp. 2262-2270
Copyright ©1999 by the American Physiological Society

Modulation of Burst Frequency, Duration, and Amplitude in the Zero-Ca2+ Model of Epileptiform Activity

Marom Bikson,1 Rahul S. Ghai,1 Scott C. Baraban,2 and Dominique M. Durand1

 1Department of Biomedical Engineering, Neural Engineering Center, and  2Department of Pediatrics and Neuroscience, Case Western Reserve University, Cleveland, Ohio 44106

Bikson, Marom, Rahul S. Ghai, Scott C. Baraban, and Dominique M. Durand. Modulation of Burst Frequency, Duration, and Amplitude in the Zero-Ca2+ Model of Epileptiform Activity. J. Neurophysiol. 82: 2262-2270, 1999. Incubation of hippocampal slices in zero-Ca2+ medium blocks synaptic transmission and results in spontaneous burst discharges. This seizure-like activity is characterized by negative shifts (bursts) in the extracellular field potential and a K+ wave that propagates across the hippocampus. To isolate factors related to seizure initiation, propagation, and termination, a number of pharmacological agents were tested. K+ influx and efflux mechanisms where blocked with cesium, barium, tetraethylammonium (TEA), and 4-aminopyridine (4-AP). The effect of the gap junction blockers, heptanol and octanol, on zero-Ca2+ bursting was evaluated. Neuronal excitability was modulated with tetrodotoxin (TTX), charge screening, and applied electric fields. Glial cell function was examined with a metabolism antagonist (fluroacetate). Neuronal hyperpolarization by cation screening or applied fields decreased burst frequency but did not affect burst amplitude or duration. Heptanol attenuated burst amplitude and duration at low concentration (0.2 mM), and blocked bursting at higher concentration (0.5 mM). CsCl2 (1 mM) had no effect, whereas high concentrations (1 mM) of BaCl2 blocked bursting. TEA (25 mM) and low concentration of BaCl2 (300 µM) resulted in a two- to sixfold increase in burst duration. Fluroacetate also blocked burst activity but only during prolonged application (>3 h). Our results demonstrate that burst frequency, amplitude, and duration can be independently modulated and suggest that neuronal excitability plays a central role in burst initiation, whereas potassium dynamics establish burst amplitude and duration.




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