Exposure to certain organophosphates (OPs) produces a delayed degeneration of the longest and largest nerve fibers (OPIDN). Until recently, investigators have used the chicken as the primary experimental model of OPIDN. Although the chicken is extremely sensitive to the ataxia associated with this neuropathy, it lacks an extensive biochemical, electrophysiological and pathological data-base. Because of this we set out to develop a rodent model of OPIDN with morphological and biochemical correlates similar to those seen in the chicken. Historically the rat had been labeled insensitive to OPIDN because of its lack of demonstrable ataxia in response to the neuropathic OPs. This paper describes the validation of a rodent model with biochemical and morphological endpoints similar to those described in the clinical and experimental literature for other models of OPIDN.
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