Effects of two pyrethroid insecticides on motor activity and the acoustic startle response in the rat

  • Kevin M. Crofton, Lawrence W. Reiter
  • Toxicology and Applied Pharmacology, September 1984, Elsevier
  • DOI: 10.1016/0041-008x(84)90214-x

Pyrethroids and Neurotoxicity

What is it about?

To better characterize the behavioral toxicity of pyrethroid insecticides, comparisons were made of the effects of cismethrin and deltamethrin exposure on motor activity and the acoustic startle response in male Long-Evans rats. Acute dose-effect, acute time course, and 30-day repeated-exposure determinations of 1-hr motor activity were made using figure-eight mazes. The acoustic startle response was measured to a 13-kHz, 120-dB(A), 40-msec tone at each of three background white noise levels (50, 65, and 80 dB). Deltamethrin (0, 2, 6, or 8 mg/kg) or cismethrin (0, 6, 12, 18, or 24 mg/kg) were administered po in 0.2 ml/kg corn oil. Cismethrin and deltamethrin produced similar dosage-dependent decreases in motor activity. The time course of onset and recovery for this decreased activity was rapid (1 to 4 hr) No cumulative effects on motor activity of a 30-day exposure to 2 mg/kg/day deltamethrin or 6 mg/kg/day cismethrin were found. The effects of cismethrin and deltamethrin on the acoustic startle response were dissimilar: deltamethrin produced a dosage-dependent decrease in amplitude and an increase in latency, and cismethrin produced an increase in amplitude and no change in latency. The differential effects of cismethrin and deltamethrin on the acoustic startle response may be related to the contrasting effects previously shown with neurophysiological and/or neurochemical techniques.

Why is it important?

The results demonstrate the ability of the acoustic startle response to differentiate between sublethal dosages of cismethrin and deltamethrin, Type I and Type II pyrethroids, respectively. Extrapolation of these effects to differentiation of the two major classes of pyrethroid insecticides will require the testing of additional compounds. Whether the etiology of these effects involves primarily actions at the GABA-receptor complex or the sodium channel remains to be determined.

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