Local cerebral glucose utilization in conscious unrestrained rats during lithium-pilocarpine - induced status epilepticus
Description
Status epilepticus (SE) is a period of continuous, prolonged electrical and behavioral seizures in which normal alert consciousness is not regained between repeated tonic-clonic attacks. Studies of SE indicate that these seizures are accompanied by large increases in both anaerobic and aerobic cerebral metabolism. A major limitation of most of these studies is that they only provide global metabolic information for the whole brain. Since the brain is not homogeneous and the function of brain is brought about by alterations in the activities of specific regions, it is likely that changes in metabolism of many specific regions may be obscured by such whole brain measurements The use of the 2-deoxyglucose (2DG) method for determining the rates of the utilization of glucose overcomes the limitations of earlier techniques since it allows for the quantitative evaluation of energy metabolism in many discrete, small regions of the brain simultaneously. The primary bases for the usefulness of the 2DG technique are that the functional activity in brain is closely coupled to the rate of energy metabolism and, in adult mammalian brain, the major substrate for energy is glucose Although a number of investigators have attempted to use the 2DG technique to examine the local cerebral glucose utilization (LCGU) of regions of brain during SE in conscious, unrestrained animals, the intensity of the seizures often result in the premature termination of the experiment and loss of experimental results Recently, a model of SE was described in rats pre-treated with lithium chloride (3 mEq/kg, i.p.) and given pilocarpine (33 mg/kg, s.c.) 24 hours later. The latency to the onset of single spikes and overt clonic seizures after the administration of pilocarpine was consistent and the seizures lasted for several hours. The most striking feature of these seizures was the absence of the excessive, violent behavioral activity often associated with convulsions, even though electroencephalographic seizures were intense. In the present study, this model was employed, together with the 2DG technique, to determine the LCGU in a number of structures in the brains of rats. The results of this study indicate that it is possible to use the 2DG method to determine the LCGU in regions of rat brain during SE. Furthermore, the pattern of LCGU indicates that the majority of structures of the limbic system and basal ganglia were more metabolically active during seizures than controls