Collombet_2008_Behav.Brain.Res_191_88

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. Accordingly, in this inaugural paper, using hemalun-phloxin staining and NeuN immunohistochemistry, the number of damaged and residual healthy neurons was quantified in the amygdala in mice over a 90-day period after soman injection (1.2LD(50) of soman). On post-soman day 1, a moderate neuronal cell death (about 23% of the whole neurons) was evidenced. In parallel, a large quantity of degenerating neurons (about 36% of the whole neurons) occurred in this brain region and survived from post-soman day 1 to day 15. The death of these damaged neurons was initiated on post-soman day 30, and ended on post-soman day 90. Concomitantly, as quantified by NeuN immunohistochemistry, a clear neuronal regeneration was demonstrated in the amygdala of soman-poisoned mice between 60 and 90 days after neurotoxicant exposure. In the companion paper (see part 2), the possible effects of both long-term neuropathology and delayed neuronal regeneration were evaluated on amygdala-driven emotional processes.