BLOCKADE OF IN VITRO ICTOGENESIS BY LOW FREQUENCY STIMULATION COINCIDES WITH INCREASED EPILEPTIFORM RESPONSE LATENCY.

Journal of neurophysiology

PubMedID: 25925325

Kano T, Inaba Y, D'Antuono M, Biagini G, Lévesque M, Avoli M. BLOCKADE OF IN VITRO ICTOGENESIS BY LOW FREQUENCY STIMULATION COINCIDES WITH INCREASED EPILEPTIFORM RESPONSE LATENCY. J Neurophysiol. 2015;jn.00248.2015.
Low frequency stimulation - delivered through transcranial magnetic or deep-brain electrical procedures - reduces seizures in patients with pharmacoresistant epilepsy. A similar control of ictal-like discharges is exerted by low-frequency electrical stimulation in rodent brain slices maintained in vitro during convulsant treatment. By employing field and 'sharp' intracellular recordings we analyzed here the effects of stimuli at 0. 1 or 1 Hz delivered in the lateral nucleus of the amyg¬dala on ictal-like epileptiform discharges induced by the K(+) channel blocker 4-aminopyridine in the perirhinal cortex (PC), in a rat brain slice preparation. We found that: (i) ictal events were nominally abolished when the stimulus rate was brought from 0. 1 to 1 Hz; (ii) this effect was associated to an increased latency of the epileptiform responses recorded in PC following each stimulus; and (iii) both changes recovered to control values following arrest of the 1 Hz stimulation protocol. The control of ictal activity by 1 Hz stimulation and the concomitant latency increase were significantly reduced by GABAB receptor antagonism. We propose that this frequency-dependent increase in latency represents a short-lasting, GABAB receptor-dependent adaptive mechanism that contributes to decrease epileptiform synchronization thus blocking seizures in epileptic patients and animal models.