Epileptiform activity and changes in field potential responses induced by low [Mg2+]0 in a genetic rat model of absence epilepsy.

The genetic absence epilepsy rats of Strasbourg (GAERS) display alterations in cortical synaptic transmission possibly facilitating the generation of ictaform activity and the late development into convulsive epilepsy. We studied low Mg2+-induced epileptiform activities and their long term effects on field potentials (fp) evoked by paired pulse stimulation in hippocampal area CA1 (CA1), medial entorhinal cortex (EC) and frontal cortex (FC) in in-vitro-slice preparations from GAERS and control (NE) adult rats (6 months). Omitting Mg2+-ions from artificial cerebrospinal fluid (ACSF) caused recurrent short discharges (in CA1) and seizure-like events (in EC) in both GAERS and NE rats. Latency to onset of activity as well as discharge pattern, frequency and amplitude of such events did not differ between the two strains, neither in CA1 nor in EC. In the FC, however, epileptiform events occurred in NE rats, but not in GAERS. Field potentials in normal ACSF were similar in both strains in CA1 and FC, while they were smaller in the EC of GAERS. Low [Mg2+]0 caused long-term changes of fp only in area CA1 where the population spikes were depressed in GAERS and increased in NE rats. We concluded that susceptibility to low [Mg2+]0-induced epileptic activity in EC and hippocampal area CA1 is not higher in GAERS than in NE adult rats. However, some properties like synaptic coupling in EC and long-term changes in synaptic efficacy induced by epileptiform activity in CA1 differ from that in NE rats. Whether the particularities in GAERS may be related to kindling by absence epileptic activities will be studied in further experiments.