Body temperature-dependent and independent actions of chlordimeform on visual evoked potentials and axonal transport in optic system of rat.
Pattern-reversal-evoked potentials (PREPs), flash-evoked potentials (FEPs), rapid axonal transport in the optic system and body temperature were measured in hooded rats, treated with either saline or the formamidine insecticide/acaricide, chlordimeform (CDM). Rats receiving chlordimeform had low body temperatures when housed at standard laboratory room temperature, 22 degrees C, but not at 30 degrees C. Peak latencies of flash-evoked potentials were prolonged by chlordimeform at 22 degrees C, but not at 30 degrees C. The rate of axonal transport was slowed in chlordimeform-treated hypothermic rats, but not in chlordimeform-treated warmed rats. These findings suggest that the flash-evoked potential and axonal transport changes produced by chlordimeform were an indirect consequence of hypothermia. In contrast, chlordimeform increased pattern-reversal evoked potential peak latencies and peak-to-peak amplitudes independent of body temperature. These findings confirm and extend previous reports of chlordimeform-induced hypothermia, emphasize the importance of changes in body temperature as a possible confounding factor in studies of neuroactive agents and demonstrate that chlordimeform has both body-temperature-dependent and independent actions in the visual system in the rat.
D000578:Amidines / Q000494:pharmacology*; D000818:Animals; D001370:Axonal Transport / Q000187:drug effects*; D001831:Body Temperature / Q000187:drug effects*; D002742:Chlorphenamidine / Q000494:pharmacology*; D005074:Evoked Potentials, Visual / Q000187:drug effects*; D006023:Glycoproteins / Q000378:metabolism; D008297:Male; D051381:Rats; D012160:Retina / Q000378:metabolism
D000578:Amidines; D006023:Glycoproteins; D002742:Chlorphenamidine