Self-sustaining status epilepticus after a brief electrical stimulation of the perforant path: a 2-deoxyglucose study

Status epilepticus remains a life-threatening condition associated with a high mortality. In order to understand the pathophysiological mechanisms underlying sustained seizures, the identification of structures involved in seizure activity allowing to define epileptic networks may be important. Thus, local cerebral metabolic rate for glucose (LCMR(glc)) was measured in a rat model of self-sustaining status epilepticus (SSSE) induced by a brief intermittent perforant path stimulation of 30 min, using the quantitative [(14)C]2-deoxyglucose autoradiographic technique. SSSE induced a generalized bilateral increase in LCMR(glcs) affecting 27 of the 42 structures studied. Largest metabolic increases (>250%) were recorded in the hippocampus, amygdala, entorhinal and piriform cortices, and lateral septum. Marked metabolic activation was also seen in basal ganglia areas such as the substantia nigra, globus pallidus and accumbens nucleus. LCMR(glcs) in brainstem, some midbrain structures, and in the neocortex were not affected by SSSE. In conclusion, a brief stimulation of the hippocampus induced a reproducible limbic SSSE in 100% of the rats, characterized by the metabolic activation of limbic and extralimbic structures, known to be involved in this type of seizures. Therefore, this new model allowing the development of a well-defined SSSE, appears to be particularly suitable for further studies on the mechanisms involved in status epilepticus.