Acute exposure to organophosphate pesticides (OPs) is associated with the development of a syndrome called organophosphate-induced delayed neuropathy (OPIDN) which is not mediated through hyper-cholinergic crisis. The present study has been designed to examine the role of alterations in dopaminergic system and neurobehavioral deficits in OPIDN. Rats were administered an acute dose of monocrotophos (MCP, 20 mg/kg body weight, orally) or dichlorvos (DDVP, 200 mg/kg body weight, subcutaneously), 15-20 min after treatment with antidotes (atropine (20 mg/kg body weight) and 2-pralidoxime (100 mg/kg body weight) intraperitoneally) to induce OPIDN. At biochemical level, an increase in dopamine, norepinephrine, and homovanillic acid levels were observed in brain of MCP- or DDVP-treated animals compared to controls. This was accompanied by increased intracellular calcium levels and lipid peroxidation in the cerebral cortex of OP-exposed animals. In addition, deficits in locomotor activity and spatial memory were observed in animals exposed to either MCP or DDVP. These results clearly suggest the role of dopaminergic system in memory and motor deficits observed in delayed neuropathy induced by OPs.
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