Abstract
Diisopropylfluorophosphate (DFP) injected into the femoral artery of cats causes a localized organophosphorus-induced delayed neuropathy (OPIDN). Gait disturbances develop in the treated leg 14 days after DFP exposure and reaches a maximum at 21 to 28 days after DFP. In vivo high-frequency conditioning of soleus motor nerve endings evokes stimulus-bound repetitive neural discharges (SBR) and an obligatory potentiation of the muscle contractile response (PTP). In this OPIDN model, SBR and PTP are maximally suppressed at 21 to 28 days after DFP. A high-dose regimen of methylprednisolone started 30 to 40 min after DFP exposure and lasting for 20 days prevented the development of OPIDN. In the methylprednisolone-DFP treated cats, SBR and PTP functions were not suppressed and not different from those in untreated normal cats.
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