Some aspects of neurophysiological basis of insecticide action.
When the insecticide parathion was administered to awake, unrestrained rats with chronically implanted brain electrodes, it was observed that the latency of the averaged flash-evoked potential in the visual cortex and superior colliculus was increased and the amplitude was decreased 2 to 4 hours later with responses returning to pretreatment levels about 8 hours after administration. Similarly, after administration of several dose levels of parathion in the rat, durations of phases of the maximal electroshock seizure (MES) pattern were altered to the greatest extent 4 hours later, but effects disappeared at 24 hours. These effects of parathion on the MES and evoked potentials coincided with a fall in blood and brain acetylcholinesterase (AChe) activities but disappeared after AChe inhibition had reached its peak and stabilized. Brain AChe activities required 2 to 4 weeks for recovery whereas blood AChe activity recovered in 1 week following inhibition by parathion (at least 2 mg/kg body weight). Studies in the monkey demonstrated similar results. Because these measurements of central nervous system function returned to normal despite continued inhibition of AChe activity, the results are interpreted to mean either that adaptation of evoked potentials or MES responses to prolonged AChe inhibition can occur in the rat and monkey after parathion administration or that some of the effects of parathion do not depend on AChe inhibition. Administration of DDT (100 mg/kg by mouth) to awake, unrestrained rats markedly increased the amplitude of spontaneous electrical activity in the cerebellum, whereas there was much less effect on electrical activity recorded simultaneously in the occipital cortex, reticular formation, and medial geniculate body. Similarly, DDT administration had marked effects on the averaged, sound evoked potential recorded in the cerebellum; DDT caused the appearance and increased the amplitude of an early component of this response not usually present during control recordings. Sound-evoked potentials recorded simultaneously from the frontal and occipital cortex and reticular formation were affected less or were decreased in amplitude by administration of DDT.
D000110:Acetylcholinesterase / Q000097:blood; D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D001921:Brain / Q000187:drug effects*; D002531:Cerebellum / Q000187:drug effects; D002800:Cholinesterase Inhibitors; D004597:Electroshock; D005071:Evoked Potentials / Q000187:drug effects; D000882:Haplorhini; D008027:Light; D008251:Macaca; D010278:Parathion / Q000633:toxicity*; D051381:Rats; D012601:Scopolamine / Q000494:pharmacology; D013016:Sound; D013116:Spinal Cord / Q000187:drug effects; D013569:Synapses / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects; D014203:Tremorine / Q000494:pharmacology; D014795:Visual Pathways / Q000187:drug effects
D002800:Cholinesterase Inhibitors; D010278:Parathion; D012601:Scopolamine; D000110:Acetylcholinesterase; D014203:Tremorine