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Electrophysiological changes in the primary sensory neuron following subchronic soman and sarin: alterations in
B D Goldstein1, D R Fincher, J R Searle
1Department of Pharmacology & Toxicology, Medical College of Georgia, Augusta 30912-3368.
Abstract:
Cats were administered soman or sarin either in a single high dose (1 mg/kg) with pretreatment or in multiple sublethal doses to determine whether these potent organophosphorus agents could produce a delayed neurotoxicity and what, if any, pathophysiological changes occurred in peripheral sensory receptors. Neither soman nor sarin, when administered as a single high dose, produced a delayed neurotoxicity as observed behaviorally for up to 60 days. There were also no observable signs of delayed neurotoxicity when these agents were administered in multiple doses. Functional tests of proprioceptors and mechanoreceptors were performed on the cats which received multiple sublethal doses of either soman or sarin. It was found that the discharge rates of muscle spindle primary endings were depressed while the discharge rates of secondary endings were facilitated following the administration of either soman or sarin. The discharge rates of slowly adapting type 1 mechanoreceptors were also depressed. The total number of identified mechanoreceptors was reduced in both the soman- and sarin-treated animals. Conduction velocities of several of the muscle spindle and mechanoreceptor afferents were significantly decreased. The alterations in muscle spindle function may be due to changes in the muscle resulting from acetylcholinesterase inhibition. Another explanation for the changes in both muscle spindle and mechanoreceptor function may be the direct effect of the organophosphorus agents on the afferents themselves, thus altering their excitability.
Insights
Organophosphorus agents soman and sarin did not cause delayed neurotoxicity in cats. However, these nerve agents altered peripheral sensory receptor function, impacting nerve conduction and receptor discharge rates.
Area of Science:
- Neuroscience
- Toxicology
- Peripheral Nervous System Research
Background:
- Organophosphorus compounds (OPCs) like soman and sarin are potent acetylcholinesterase inhibitors.
- Potential for delayed neurotoxicity and peripheral nerve damage from OPC exposure requires thorough investigation.
Purpose of the Study:
- To determine if soman or sarin induce delayed neurotoxicity in cats.
- To investigate pathophysiological changes in peripheral sensory receptors following exposure to soman or sarin.
Main Methods:
- Cats were administered single high doses or multiple sublethal doses of soman or sarin.
- Functional tests assessed proprioceptors and mechanoreceptors.
- Electrophysiological measurements evaluated afferent nerve conduction velocities and discharge rates.
Main Results:
- No behavioral signs of delayed neurotoxicity were observed after single high or multiple sublethal doses.
- Significant alterations in muscle spindle primary and secondary ending discharge rates were noted.
- Slowly adapting type 1 mechanoreceptor discharge rates were depressed, and the total number of mechanoreceptors decreased.
- Conduction velocities of muscle spindle and mechanoreceptor afferents were significantly reduced.
Conclusions:
- Soman and sarin did not produce observable delayed neurotoxicity in cats.
- Organophosphorus agent exposure significantly altered peripheral sensory receptor function.
- Observed changes may result from acetylcholinesterase inhibition or direct effects on nerve afferents.
