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BRAIN CHOLINESTERASE INHIBITION PRODUCED BY PROPOXUR AND DEPRESSION OF THE PHOTIC AFTER DISCHARGE OF FLASH EVOKED POTENTIALS IN LONG EVANS RATS.
Citation:
MWANZA, J., J. GRAFF, C. SPIVEY, AND D. W. HERR. BRAIN CHOLINESTERASE INHIBITION PRODUCED BY PROPOXUR AND DEPRESSION OF THE PHOTIC AFTER DISCHARGE OF FLASH EVOKED POTENTIALS IN LONG EVANS RATS. Presented at Society of Toxicology, Charlotte, NC, March 25 - 29, 2007.
Description:
Propoxur is a widely used N-methyl carbamate pesticide that acts by inhibiting cholinesterases (ChE), which may lead to cholinergic toxicity. Flash evoked potentials (FEPs) are a neurophysiological response following stimulation of the visual system with flashes of light. They are often used to detect central nervous system (CNS) changes following exposure to neurotoxic compounds. Disruption of CNS function by ChE inhibitors produced decreases in the photic after discharge (PhAD) of the FEP. The PhAD is related to higher cortical processing of visual information. To determine the dose-response for propoxur on the PhAD, FEPs were recorded in adult male Long-Evans rats after oral gavage with propoxur 0, 0.3, 3, 10, 20, 30 or 40 mg/kg (corn oil vehicle). One week before testing, rats were implanted with electrodes over the visual cortex and allowed to recover. FEPs were recorded for 2 consecutive days to familiarize the rats with the test procedure and to develop the PhAD. On the 3rd day, pupils were dilated (40 min) and animals dosed (30 min) before testing. Immediately after testing, rats were sacrificed, and the brains removed and stored at -80oC, until determination of brain ChE levels by a radiometric assay. All doses greater than 0.3 mg/kg of propoxur significantly inhibited brain ChE. Three-40 mg/kg propoxur inhibited 38-63% of brain ChE. The duration of the PhAD was significantly decreased at 30 mg/kg by 54%. A correlation was obtained between brain ChE levels and the PhAD duration. A significant decrease in colonic temperature was observed at 10, 20 and 40 mg/kg propoxur. Treatment with 40 mg/kg propoxur increased the latency of peak N166. No effect on the latency and amplitude of early components of the FEP was observed. These results indicate that ChE inhibition produced by propoxur disrupts the cortical processing related to the later portion of the FEP. 1Supported by a NRC Fellowship. This is an abstract of a proposed presentation and does not necessarily reflect EPA policy.