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RECORD NUMBER: 33 OF 60

OLS Field Name OLS Field Data
Main Title Increased Hippocampal Excitability Produced by Amitraz (Journal Version).
Author Gilbert, M. E. ; Dyer, R. S. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. ;Northrop Services, Inc./Environmental Sciences, Research Triangle Park, NC.
Publisher c1988
Year Published 1988
Report Number EPA/600/J-88/158;
Stock Number PB89-110555
Additional Subjects Toxicology ; Pesticides ; Hippocampus ; Central nervous system ; Neural transmission ; Evoked potentials ; Laboratory animals ; Reprints ; Amitraz ; Toxic substances ; Methanimidamide/N'-dimethyphenyl-N-dimethyphenyl-iminomethyl-N-methyl
Holdings
Library Call Number Additional Info Location Last
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Status
NTIS  PB89-110555 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 03/14/1989
Collation 8p
Abstract
The study characterized the effect of the formamidine pesticide, amitraz, upon hippocampal function in male Long Evans rats. Animals were chronically prepared with a stimulating electrode in the perforant path and field potentials were recorded from a bipolar electrode situated across the granule cell layer of the dentate gyrus. Input/output functions and paired pulse inhibition were monitored in unrestrained, unanesthetized animals over a number of days following acute administration of 100 mg kg of amitraz. Inout/output functions revealed a decrease in excitatory postsynaptic potential (EPSP) slope and an increase in population spike height 4 and 24 hr after treatment, with return to baseline by 48 hr. Tests of inhibition using pairs of stimulus pulses delivered at intervals ranging between 20 and 100 msec revealed a decrease in inhibition following amitraz. Both of these effects could be mimicked by administration of 0.1 mg/kg of the alpha-2 agonist clonidine, supporting this mode of action of amitraz on CNS function. The results indicate that systemic amitraz treatment produced a transient enhancement of excitatory and reduction of inhibitory processes in a CNS pathway.