Eukaryotic DING proteins are endogenous: an immunohistological study in mouse tissues.

Background: DING proteins encompass an intriguing protein family first characterized by their conserved N-terminal sequences. Some of these proteins seem to have key roles in various human diseases, e.g.

Effects of soman poisoning on mitochondrial respiratory enzyme activity in the mouse hippocampus and cerebral cortex.

Mitochondrial dysfunctions have been highlighted as a contributing factor in epileptic seizures and subsequent neuronal cell death. Soman is an irreversible inhibitor of cholinesterase, triggering epileptic seizures leading to massive neuronal cell death in brain areas, such as the hippocampus and cerebral cortex. Mitochondrial respiratory chain enzymatic assays were performed in hippocampus and cerebral cortex homogenates from mouse brains collected 3 hours, 24 hours, 3 days, and 7 days after soman poisoning.

Long-term consequences of soman poisoning in mice Part 1. Neuropathology and neuronal regeneration in the amygdala.

To date, studies on soman-induced neuropathology mainly focused on the hippocampus, since this brain region is a well-delimited area with easily detectable pyramidal neurons. Moreover, the hippocampus is severely damaged after soman exposure leading to a substantial alteration of behavioral mnemonic processes. The neuropathology described in the hippocampus, however, and its behavioral consequences cannot be extrapolated to all other limbic damaged brain areas such as the amygdala.

Long-term behavioral consequences of soman poisoning in mice.

We investigated the long-term (up to 90 days) consequences of soman intoxication in mice on weight, motor performances (grip strength, rotarod) and mnemonic cognitive processes (T-maze, Morris water maze test). First, a relative weight loss of 20%, measured 3 days after intoxication, was evidenced as a threshold beyond which neuropathological damage was observed in the hippocampus. Animals were then distributed into either low weight loss (LWL) or high weight loss (HWL) groups according to the relative 20% weight loss threshold.

Soman poisoning induces delayed astrogliotic scar and angiogenesis in damaged mouse brain areas.

Gliotic scar formation and angiogenesis are two biological events involved in the tissue reparative process generally occurring in the brain after mechanically induced injury, ischemia or cerebral tumor development. For the first time, in this study, neo-vascularization and glial scar formation were investigated in the brain of soman-poisoned mice over a 3-month period after nerve agent exposure (1.2 LD50 of soman).