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EPSP depression following neocortical seizures in cat
Author(s) -
Nita Dragos A.,
Cissé Youssouf,
Timofeev Igor
Publication year - 2008
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2007.01431.x
Subject(s) - excitatory postsynaptic potential , neuroscience , postsynaptic potential , stimulation , electrophysiology , cats , epilepsy , barbiturate , anesthesia , neurotransmission , neocortex , medicine , psychology , inhibitory postsynaptic potential , receptor
SummaryTo study the possible mechanism(s) underlying unresponsiveness following neocortical seizures, we recorded excitatory postsynaptic potentials (EPSPs) of cortical neurons evoked by ipsilateral cortical stimulation before and after spontaneous or elicited seizures. Regular‐spiking neurons (n = 32) were intracellularly recorded in association area five of cats under ketamine–xylazine or barbiturate anesthesia. Compared with control responses, cortically evoked EPSPs were characterized by decreased amplitude after electrographic seizures. Synaptic responses and intrinsic properties were measured by applying extracellular electrical stimuli followed by intracellular hyperpolarizing current pulses. The input resistance decreased during seizures but quickly recovered to control level after the paroxysms, whereas the amplitude of evoked EPSPs remained lower following seizures, generally for 2–12 min, suggesting that the decreased EPSPs were not due to an alteration of intrinsic response. Data demonstrate a long‐lasting decreased synaptic responsiveness following generalized spike‐wave seizures slowly recovering in time.