Pattern reversal evoked potentials (PREPs), flash evoked potentials (FEPs), optic nerve axonal transport, and body temperature were measured in hooded rats treated with either saline or the formamidine insecticide/acaricide, chlordimeform (CDM). Rats receiving CDM had low body temperatures when housed at standard laboratory room temperature, 22C, but not at 30C. FEP peak latencies were prolonged by CDM at 22C, but not at 30C. The rate of axonal transport was slowed in CDM-treated hypothermic rats, but not in CDM-treated warmed rats. These findings suggest that the FEP and optic nerve axonal transport changes produced by CDM were a secondary consequence of hypothermia. In contrast, CDM produced increased PREP peak latencies and peak-to-peak amplitudes which were independent of body temperature. These findings confirm and extend previous reports of CDM-induced hypothermia, emphasize the importance of body temperature changes as a possible confounding factor in studies of neuroactive agents, and demonstrate that CDM has both body-temperature dependent and independent actions in the rat visual system.