Release of amino acids from chronic epileptic and subepileptic foci in vivo.

Perforated discs of cobalt or nickel were implanted onto the sensorimotor strip of the cerebral cortex of rats. Co discs gave rise to myoclonic contralateral limb-jerks in a manner similar to Co powder lesions. In contrast, Ni-implanted animals were never observed to show overt limb-jerks. On superfusion with an in vivo cannula system, both types of lesion released increased amounts of glutamate, valine and glycine as compared with unlesioned tissue. However, the enhancement of release from epileptogenic Co lesions was approximately 3-fold greater than that from non-epileptogenic lesions. In addition, epileptogenic lesions showed a marked reduction in glutamine release compared to controls, while non-epileptogenic lesions did not. The possible involvement of local disorders of the glutamate/glutamine system in the generation of cobalt focus hyperactivity is discussed.