The seizure state induced in the rat by cerebral cortical implantation of
cobalt metal has been increasingly used to study a variety of neurochemical parameters. This experimental model of
epilepsy affords the opportunity to study events prior to the development of
seizures, during the period of intense seizure activity, and during the period when seizure activity has essentially terminated. The
seizures that occur in this model are intermittent and paroxysmal and share many other similarities with human
epilepsy. The crucial question with this model, and indeed with any experimental model of
epilepsy, is whether the basic seizure-producing mechanism(s) is similar. This question remains to be answered. There have been studies that show that changes in certain neurochemical parameters parallel the onset, intensity, and decline of seizure activity in
cobalt-epileptic animals. Although extremely interesting, by themselves they do not prove a cause-and-effect relationship. Such parallelism is more apparent in the case of
GABA than in the cases of
lipids and
gangliosides.
GABA and its synthetic
enzyme,
glutamic acid decarboxylase (GAD), are both at normal levels prior to the development of
seizures, are significantly decreased during the period of
seizures, and return toward control values at a time when
seizures are no longer apparent. On the other hand, there is no change in postsynaptic
GABA binding sites (Bmax) prior to
seizures, a significant increase in Bmax during seizure activity, and a return toward normal by 21 days (when seizure activity has terminated). Studies that have been carried out on
lipids and
gangliosides in
cobalt-induced
epilepsy are not nearly as extensive nor are the results as positive as those that have been obtained in the case of
GABA. They do, however, provide provocative findings that may well be related to the genesis of
epilepsy.