INSERM U 398, Université Louis Pasteur, Strasbourg, France

Correspondence: Astrid Nehlig, INSERM U 398, Faculté de Médecine, 11 rue Humann, 67085 Strasbourg Cedex, France.

¹Dr. Maria José S. Fernandes is a postdoctoral fellow sponsored by Conselho Nacional de Desenuoluimento Cientifico e Technologico and Fundaçao de Amparo a Pesquisa do Estado de Sao Paulo. Her present address is Disciplina de Neurologia Experimental, Universidade Federal de Sao Paulo-Escola Paulista de Medicina, Rua Botucatu, 862, Sao Paulo, SP, Brazil.

Received 23 January 1998; Revised 27 April 1998; Accepted 26 May 1998.

Abstract

The correlation between seizure-induced hypermetabolism and subsequent neuronal damage was studied in 10-day-old (P10), 21-day-old (P21), and adult rats subjected to lithium-pilocarpine status epilepticus (SE). Local CMR_glc (LCMR_glc) values were measured by the [¹⁴C]2-deoxyglucose method for a duration of 45 minutes starting at 60 minutes after the onset of SE, and neuronal damage was assessed by cresyl violet staining at 6 days after SE. In P21 and adult rats, LCMR_glc values were increased by 275 to 875% in all thalamic, cortical, forebrain, and hypothalamic regions plus the substantia nigra. In addition, at P21 there were also large increases in LCMR_glc in brainstem regions. In P10 rats, metabolic increases were mostly located in cortical and forebrain regions plus the substantia nigra but did not affect hypothalamic, thalamic, or brainstem areas. In adult rats, there was an anatomical correlation between hypermetabolism and neuronal damage. At P21, although hypermetabolism occurred in regions with damage, the extent of damage varied considerably with the animals and ranged from an almost negligible to a very extended degree. Finally, in P10 rats, although quite pronounced hypermetabolism occurred, there was no neuronal damage induced by the seizures. Thus, in the present model of epilepsy, the correlation between marked hypermetabolism and neuronal damage can be shown in adult rats. Conversely, immature rats can sustain major metabolic activations that lead either to a variable extent of damage, as seen at P21, or no damage, as recorded at P10.