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The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 274-280
Copyright ©2000 by the American Physiological Society
Neural Engineering Center, Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44106
Ghai, Rahul S.,
Marom Bikson, and
Dominique M. Durand.
Effects of Applied Electric Fields on Low-Calcium Epileptiform
Activity in the CA1 Region of Rat Hippocampal Slices. J. Neurophysiol. 84: 274-280, 2000. It is
well established that exogenous electric fields can suppress activity
obtained in different models of epileptiform discharge such as
penicillin and high potassium. In the low-calcium model of epilepsy,
spontaneous epileptiform bursting is generated in the absence of
synaptic transmission. It has been suggested that ephaptic
interactions play a critical role in neuronal synchronization and burst
propagation in this nonsynaptic model. We, therefore, tested the
hypothesis that low-calcium bursting induced in the CA1 region of
transverse and longitudinal hippocampal slices should be highly
sensitive to exogenous electric fields. Uniform, low amplitude DC
electric fields were applied during spontaneous low-calcium epileptiform activity. Modulation and full suppression of epileptiform activity was observed at field strengths between 1 and 5 mV/mm, a value
significantly lower than in other in vitro models of epilepsy. We
further investigated the hypothesis that the efficacy of electrical fields was related to changes in the extracellular space. Our results
suggest that the osmolality of the perfusate can modulate the efficacy
of electric fields. It was also observed that the ability of a field to
suppress or modulate low-calcium activity was highly dependent on its
orientation, polarity, as well as magnitude. Finally, it was observed
that the extracellular potassium "waves" that normally accompany
individual epileptiform events was abolished when the individual events
were suppressed. These results suggest that DC fields modulate and
suppress low-calcium activity by directly polarizing CA1 pyramidal cells.
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