[Stem-cell engraftment as delayed therapy to repair organophosphate-induced brain damage]. / Utilisation potentielle des greffes de cellules souches pour le traitement différé des lésions cérébrales induites par les neurotoxiques organophosphorés.

Amongst organophosphate compounds, both pesticides and warfare neurotoxics are probably the most representative. These compounds are irreversible acetylcholinesterase inhibitors. Usual clinical signs observed after acute poisoning are mainly respiratory distress, convulsions and seizures. Following acute poisoning, an emergency treatment must be provided as soon as possible (maximum delay of 1 hour post-poisoning), to prevent irreversible brain damage and patient death. At the present time, there is no efficient delayed treatment which could be provided if this 1 hour latency is overpassed. However, neurogenesis by stem cell engraftment, eventually complemented by gene therapy strategy, could be a potential therapeutic approach to repair organophosphate-induced brain damage. Main stem cell engraftement strategies successfully used for brain damage of various origins are reviewed in this Article.

Acute exposure to a low or mild dose of soman: biochemical, behavioral and histopathological effects.

Effects of low to mild doses of soman on central and blood cholinesterase (ChE) activities and anxiety behavior were studied in mice 30 min, 24 h and 7 days after poisoning. At these two latter time points, histopathological consequences of soman intoxication were also studied. The 30-microg/kg dose of soman produced 30 min after intoxication, about 35% of central ChE inhibition, and an anxiolytic effect without toxic signs or histopathological changes. The 50-microg/kg dose of soman produced at the same time, about 56% of central ChE inhibition, slight clinical signs of poisoning without convulsions, an anxiogenic effect with a slight hypolocomotion but no brain damage. A mild dose of soman (90 microg/kg) produced at this same time point about 80% of central ChE inhibition, and led to ataxia and tremors in every mouse and to convulsions in some of them. Thirty minutes and 24 h after poisoning, the behavioral tests revealed neither anxiolytic nor anxiogenic responses despite a clear hypolocomotion. Only mice that experienced long-lasting convulsions developed neuropathological changes. The functional implication of our results, as well as the biological relevance of blood vs. brain ChE levels, as an index of intoxication severity are discussed.

[Changes of the course of experimental epileptic attacks by curarization]. / Modification de l'évolution de crises comitales expérimentales par la curarisation.

In our studies on the Rabbit, the time of seizure in increase after curarization. The curare do not pass through the blood brain barrier ; the action of drug can not be a direct action on the central nervous system.