DOES PROLONGED IMPLANTATION OF DEPTH ELECTRODES PREDISPOSE THE BRAIN TO KINDLING

Chronically implanted depth electrodes are widely used for the study o f electrical signals generated in deep cerebral locations and for elec trical stimulation of such locations. Although the effects of lesions resulting from electrode implantation are generally considered minimal , some reports have shown lasting neurochemical, histological, and beh avioral alterations in response to such implantation. Furthermore, the re is some evidence that prolonged electrode implantation may decrease the seizure threshold of the implanted region and increases the rate of kindling from this region. This prompted us to undertake a study on different periods of post-surgical delay to onset of electrical stimu lation and subsequent characteristics of kindling development. Rats we re implanted with a bipolar electrode in the basolateral amygdala, and the threshold for induction of focal paroxysmal activity (afterdischa rge threshold, ADT) was determined after post-surgical recovery period s of either 1, 2, 4, or 8 weeks. The animals were then kindled by dail y administration of an electrical stimulus until all rats exhibited fu lly kindled seizures. In fully kindled rats, the ADT was redetermined. Compared to animals with 1 week of electrode implantation, the pre-ki ndling ADT was significantly lower in rats with 2 and 4 weeks of elect rode implantation, but returned towards the 1 week values at 8 weeks. An enhanced kindling rate was seen when kindling stimulations were sta rted after 4 and 8 weeks of electrode implantation. Despite the marked differences in pre-kindling ADT, the post-kindling ADT was similar in the groups with 1, 2, or 4 weeks but significantly lower in the group with 8 weeks post-surgical delay to onset of testing. The data sugges t that prolonged implantation of a bipolar electrode into a sensitive region of the limbic system predisposes the brain to kindling. Based o n previous observation of iron deposits induced by electrode implantat ion and the epileptogenic effect of iron in cortical and limbic region s, we propose that the present observations are due to deposition of i ron from hemoglobin destruction in local microhemorrhages caused by th e implantation.