Organophosphorus Ester-Induced Delayed Neurotoxicity: Pathophysiological Alterations in the Primary Sensory Neuron

摘要

The present study was carried out to determine the effects of the organophosphorous agents soman and sarin on the primary sensory neuron to determine in particular, whether these agents will produce a delayed neurotoxicity and if not, whether they still affect sensory processing in the periphery and spinal cord. It was found that neither soman nor sarin could produce a classical delayed neurotoxicity at the doses and times used in these studies. However, certain aspects of primary afferent function were still affected by these agents. These changes include effects on cutaneous mechanoreceptors, muscle spindle function, and spinal cord reflexes. Soman had no effect on muscle spindles but did reduce the number of mechanoreceptors. Sarin, on the other hand, depressed the response of primary endings and increased the response of secondary endings to stretch. Sarin also reduced the number of mechanoreceptors present in the tibial nerve. Both soman and sarin depressed the monosynaptic reflex (MSR) and L7-evoked dorsal root reflex (DRR). However, only the soman seems to depress significantly the antidromic outputs of the dorsal root when evoked from the peripheral nerves. These data show that soman and sarin can adversely affect the physiological parameters of proprioception and cutaneous sensation at low level, subchronic dosing. The extent of these deficits is serious. However, there is no neurological impairment at the time of the experiments. It is unclear as to whether these changes can lead to neurological impairment or whether they are reversible.