Peripheral neuropathy was induced by the long-term administration of organo-phosphorus compounds (phtalimid/phosmet) in quails (Coturnix coturnix japponica). After 4 weeks, the first symptoms of organophosphorus (OPC) poisoning (apathy, diarrhea) were present. During the second month of a daily administration of the toxic substance using the probe, an apparent clinical autonomic and peripheral neuropathy with ataxia had developed. Toxic disturbance of the nervous system was confirmed by the examination of spinal and cortical somatosensory evoked potentials (SEP) after tibial nerve stimulation. The prolongation of the peripheral conduction time (wave P6 and N9 represent the response from the ischiadic nerve and the entry of the stimulus to spinal cord, respectively) confirmed a peripheral nerve lesion. We suggest that these clinical and electrophysiological changes, displayed by the disturbed nervous system, are caused by either slowing or stoppage of the axonal flow, transport of proteins and other substances, as well as by axon demyelination (Tab. 1, Fig. 1, Ref. 22).