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Journal of Neuroscience, Vol 15, 3110-3117, Copyright © 1995 by Society for Neuroscience
Selective increase in T-type calcium conductance of reticular thalamic neurons in a rat model of absence epilepsy
E Tsakiridou, L Bertollini, M de Curtis, G Avanzini and HC Pape
Abteilung fur Neurophysiologie, Medizinische Fakultat, Ruhr- Universitat, Bochum, Germany.
The properties of voltage-dependent calcium currents were compared in
thalamic neurons acutely dissociated from a rat model of absence epilepsy,
designated as Genetic Absence Epilepsy Rat from Strasbourg (GAERS), and
from a Nonepileptic Control strain (NEC). Two populations of neurons were
isolated: thalamocortical relay neurons of the nucleus ventrobasalis (VB)
and neurons of the nucleus reticularis (RT) of the thalamus. Whole-cell
patch-clamp analysis demonstrated an increase in the amplitude of the
calcium (Ca2+) current with a low threshold of activation (IT) in RT
neurons of GAERS in comparison to that of the seizure-free rat strain (-198
+/- 19 pA and -128 +/- 14 pA, respectively), whereas the sustained
component (IL) was not significantly different. The kinetic properties,
voltage dependence, and basic pharmacological sensitivity of the Ca2+
conductances were similar in the two populations of neurons. The amplitude
of both IT and IL in RT neurons increased after birth, and differences in
IT between GAERS and NEC attained significance after postnatal day 11. At
corresponding ages, the Ca2+ currents in VB thalamocortical relay neurons
were not altered in GAERS in comparison to those in NEC. We conclude that
the selective increase in IT of RT neurons enhances the probability of
recurrent intrathalamic burst activity, thereby strengthening the
synchronizing mechanisms in thalamocortical systems, and, as such,
represents a possible primary neuronal dysfunction that relates to the
pathological increase in synchronization underlying the generation of
bilateral and synchronous spike and wave discharges (SWDs) in an
established genetic model of generalized epilepsy.
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[Abstract]
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