Status epilepticus affects the gigantocellular network of the pontine reticular formation.

Background: The impairment of the pontine reticular formation (PRF) has recently been revealed to be histopathologically connected with focal-cortical seizure induced generalized convulsive status epilepticus. To elucidate whether the impairment of the PRF is a general phenomenon during status epilepticus, the focal-cortical 4-aminopyridine (4-AP) application was compared with other epilepsy models. The presence of "dark" neurons in the PRF was investigated by the sensitive silver method of Gallyas in rats sacrificed at 3 h after focal 4-AP crystal or systemic 4-AP, pilocarpine, or kainic acid application.

The mode of death of epilepsy-induced "dark" neurons is neither necrosis nor apoptosis: an electron-microscopic study.

Morphological aspects of the formation and fate of neurons that underwent dramatic ultrastructural compaction ("dark" neurons) induced by 4-aminopyridine epilepsy were compared in an excitotoxic and a neighboring normal-looking area of the rat brain cortex. In the excitotoxic area, the later the ultrastructural compaction began after the outset of epilepsy, the higher the degree of mitochondrial swelling and ribosomal sequestration were; a low proportion of the affected neurons recovered in 1 day; the others were removed from the tissue through a necrotic-like sequence of ultrastructural changes (swelling of the cell, gradual disintegration of the intracellular organelles and dispersion of their remnants into the surroundings through large gaps in the plasma and nuclear membranes). In the normal-looking area, the ultrastructural elements in the freshly-formed "dark" neurons were apparently normal; most of them recovered in 1 day; the others were removed from the tissue through an apoptotic-like sequence of ultrastructural changes (the formation of membrane-bound, electrondense, compact cytoplasmic protrusions, and their braking up into membrane-bound, electrondense, compact fragments, which were swallowed by phagocytotic cells).