G. Vanostrand et Rm. Cooper, [C-14] 2-DEOXYGLUCOSE AUTORADIOGRAPHIC TECHNIQUE PROVIDES A METABOLICSIGNATURE OF COBALT-INDUCED FOCAL EPILEPTOGENESIS, Epilepsia, 35(5), 1994, pp. 939-949
Brain glucose consumption in rats with unilateral visual cortex implan
ts 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 aroun
d the implant site. The dark patches were located just beyond the dama
ged perifocal zone, in normal-appearing Nissl-stained cortex designate
d by the electrocorticographic (ECoG) work of other investigators as t
he focus of epileptic activity. As was also predictable from earlier r
esearch, the cortical patches were prominent on day 9 and absent by da
y 35. Regions of high metabolic activity in thalamus, presumably the r
esult 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 similar to 36
5, may account for the persistent sensitivity to seizure-inducing drug
s that occurs secondary to cobalt implants. The absence of dark patche
s after control nonseizure-inducing but toxic copper implants argued a
gainst the possibility that the dark patches reflected some nonepilept
ogenic effect of the cobalt. As well, under pentobarbital anesthesia,
the patches behaved in a manner suggesting that their 2-DG uptake refl
ected neural and not glial cell activity. Dark patches are a distincti
ve autoradiograph signature of tissue made epileptic by cobalt.