METABOLIC BASIS FOR THE SELECTIVE VULNERABILITY OF NEURONS IN STATUS EPILEPTICUS

Unstarved, male Wistar rats (290–410 g) were anesthetized with 2–3% halothane, tracheotomized, and connected to a respirator delivering 70% N20 and 30% 02. Catheters were placed in the femoral arteries and in one femoral vein. Gold‐plated screws were inserted in the skull bone for recording of (frontoparietal) EEG. When the operative procedures were completed, halothane supply was discontinued. Arterial PCO2 was adjusted to 35–40 mmHg, and body temperature was maintained close to 37oC. The animals were allowed a steady state period of about 30 min before seizures were induced by the i.v. injection of bicuculline (1.2 mg‐kg‐1, see Chapman et al. 1977). Just before the injection the animals were bled to a mean arterial blood pressure of about 120 mmHg to avoid too excessive an increase in pressure at the onset of seizures. Local CMRg1 was determined with the method described by Sokoloff et al. (1977). In summary, after 20 min of seizure activity 1 ml of a 14C‐deoxyglucose solution (New England Nuclear), containing 30 μCi, was injected i. v. Over the next 30 min, repeated arterial blood samples were taken for determination of plasma glucose concentration (hexokinase method) and ,4C activity (liquid scintillation counting). At the end of this period, the animals were decapitated and the brains were prepared for quantitative autoradiography. Local CMRgl was calculated from the integrated plasma activity and from the 14C activity in tissue. The latter was determined from the X‐ray films by microdensitometry, either manually (see Abdul‐Rahman et al. 1979) or, in one case, with the automatic microscanning equipment developed in the Laboratory of Cerebral Metabolism, NIMH, Bethesda (courtesy of Dr Louis Sokoloff). © 1979 Scandinavian Physiological Society