Chlorine conductance of the GABAA receptor of synaptoneurosomes from the brain cortex of WAG/Rij rats with absence epilepsy and wistar rats at an early period in the development of nonconvulsive or tonic-clonic kindling

We have studied muscimol-induced 36Cl− conductivity in synaptoneurosomes prepared from the frontal and somatosensory cortex of rats with three types of epileptic activity: tonic-clonic pentylenetetrazole kindling in Wistar rats, nonconvulsive absence pentylenetetrazole kindling in Wistar rats, and a genetic model of epilepsy in WAG/Rij rats. We used two concentrations of muscimol: 30 and 100 μM. The occurrence of kindling prior to tonic-clonic seizures in the Wistar rats was considerably decreased in the muscimol-induced 36Cl− conductivity as compared to the control. Development of nonconvulsive kindling considerably increased the 36Cl− conductance into the neocortical synaptoneurosomes. The control WAG/Rij rats demonstrated a significant increase in the 36Cl− conductance into neocortical synaptoneurosomes as compared to the control Wistar rats. The decrease in muscimol-induced 36Cl− conductivity after development of tonic-clonic kindling was in agreement with a large volume of literature data regarding the decrease in the activity of GABAA receptor during tonic-clonic kindling. The high level of muscimol-induced 36Cl− conductivity in the neocortical synaptoneurosomes of the WAG/Rij rats supported the concept that absence epilepsy was induced by hyperpolarization. The high level of 36Cl− conductivity during nonconvulsive pentylenetetrazole-induced kindling suggested that the activity of the GABAA receptor was similar in the genetic and drug-induced models of the absence epilepsy.