Genetic absence epilepsy rats from Strasbourg (GAERS) have non-convulsive generalized seizures associated with spike-wave (SW) discharges, which are due to a hyperexcitable state of the thalamo-cortico circuits involving the reticular thalamic nucleus (nRt). Investigation of the primary genetically-determined defect responsible for GAERS epilepsy revealed the following abnormalities: (1) increased effectiveness of AMPA receptors dependent glutamate-mediated transmission; (2) impairment of GABA-mediated transmission in the neocortex; (3) increased amplitude of the voltage-dependent low-threshold Ca2(+)-current (I(T)) in the nRt. The maturational profile of these abnormalities supports the conclusion that the abnormality in the I(T) current in the nRt is the primary genetically-determined defect, which may secondarily induce the other changes found in the neocortex and thalamus of GAERS.
Avanzini, G., de Curtis, M., Franceschetti, S., Sancini, G., Spreafico, R. (1996). Cortical versus thalamic mechanisms underlying spike and wave discharges in GAERS. EPILEPSY RESEARCH, 26(1), 37-44 [10.1016/S0920-1211(96)00037-X].
Cortical versus thalamic mechanisms underlying spike and wave discharges in GAERS
SANCINI, GIULIO ALFREDO;
1996
Abstract
Genetic absence epilepsy rats from Strasbourg (GAERS) have non-convulsive generalized seizures associated with spike-wave (SW) discharges, which are due to a hyperexcitable state of the thalamo-cortico circuits involving the reticular thalamic nucleus (nRt). Investigation of the primary genetically-determined defect responsible for GAERS epilepsy revealed the following abnormalities: (1) increased effectiveness of AMPA receptors dependent glutamate-mediated transmission; (2) impairment of GABA-mediated transmission in the neocortex; (3) increased amplitude of the voltage-dependent low-threshold Ca2(+)-current (I(T)) in the nRt. The maturational profile of these abnormalities supports the conclusion that the abnormality in the I(T) current in the nRt is the primary genetically-determined defect, which may secondarily induce the other changes found in the neocortex and thalamus of GAERS.
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