Neuropsychobehavioural toxicodynamics of imidacloprid–a nitroguanidine insecticide
Abstract
The present investigation was designed to study the neuropsychobehavioural toxicodynamics of imidacloprid, a nitroguanidine insecticide, in adult swiss albino male mice and wistar rats.
Following intraperitoneal administration of imidacloprid in mice, the main gross observable symptoms were decreased alertness, decreased grooming, restlessness, tremors, respiratory distress, abnormal body posture, open mouth breathing and flexion of head. No muscarinic effects were observed.
The maximal tolerated dose of imiodacloprid was 55 mg/kg, i.p. Imidacloprid decreased spontaneous motor activity in a dose dependent manner and induced motor incoordination. It antagonized cocaine and amphetamine induced behaviour. Imidacloprid potentiated the seizures induced by electroshock, pentylenetetrazole, strychnine, tremorine and picrotoxin to tonic convulsions or death. It decreased the severity of lithium pilocarpine induced status epilepticus but increased the severity of status epilepticus induced by phenytoin pentylenetetrazole to tonic convulsions. Imidacloprid prolonged the barbiturates induced hypnosis. Prior administration of diazepam and carbamazepine decreased the tremors and prior administration of phenytoin reduced the restlessness induced by imidacloprid. However, prior treatment with fluoxetin had no effect on imidacloprid induced characteristic behavioural symptoms. Imidacloprid did not behave exactly like nicotine. It possess no autonomic muscarinic action. Effect of imidacloprid indicated the possibility of involvement of dopaminergic system and direct excitatory action at neuromuscular junction.