Abstract
The GABA-withdrawal syndrome (GWS)
is a model of local status epilepticus following
the interruption of a chronic GABA infusion
into the rat somatomotor cortex. GWS is
characterized by focal epileptic electroencephalographic
discharges and associated contralateral
myoclonus. In neocorticai slices obtained
from GWS rats, most neurons recorded in the
GABA-infused area are pyramidal neurons
presenting bursting properties. The bursts are
induced by white-matter stimulation and/or
intracellular depolarizing current injection
and correlate with a decrease of cellular
sensitivity to GABA, caused by its prolonged
infusion. This effect is related to a calcium
influx that may reduce the