14C]2-deoxyglucose autoradiographic technique provides a metabolic signature of cobalt-induced focal epileptogenesis.

Abstract

Brain glucose consumption in rats with unilateral visual cortex implants of epileptogenic cobalt rods was assessed by the 2-deoxyglucose (2-DG) method. Nine days postoperatively, "dark patches" of higher 2-DG uptake, bordered by tissue showing lesser uptake, were observed around the implant site. The dark patches were located just beyond the damaged perifocal zone, in normal-appearing Nissl-stained cortex designated by the electrocorticographic (ECoG) work of other investigators as the focus of epileptic activity. As was also predictable from earlier research, the cortical patches were prominent on day 9 and absent by day 35. Regions of high metabolic activity in thalamus, presumably the result of axonal transport of cobalt ions, were also strikingly evident in the projection nuclei connecting with the cortical implant sites. The abnormal thalamic activity is likely the metabolic counterpart of "secondary foci," a characteristic feature of the cobalt model. The longevity of these thalamic dark patches, which developed between days 2 and 9 and did not disappear until between days 90 and approximately 365, may account for the persistent sensitivity to seizure-inducing drugs that occurs secondary to cobalt implants. The absence of dark patches after control nonseizure-inducing but toxic copper implants argued against the possibility that the dark patches reflected some nonepileptogenic effect of the cobalt. As well, under pentobarbital anesthesia, the patches behaved in a manner suggesting that their 2-DG uptake reflected neural and not glial cell activity. Dark patches are a distinctive autoradiograph signature of tissue made epileptic by cobalt.