© 1996 Oxford University Press
research-article |
Characterization of Olfactory Deficits in the Rat Following Administration of 2,6-Dichlorobenzonitrile (Dichlobenil), 3,3'-Iminodipropionitrile, or Methimazole1,2
*Department of Toxicology, North Carolina State University Raleigh, North Carolina 27695-7633
Neurotoxicology Division, U.S. Environmental Protection Agency Research Triangle Park, North Carolina 27711
Received December 12, 1994; accepted June 26, 1995
The histopathology of the olfactory mucosal lesion associated with ip adminstration of 2,6-dichlorobenzonitrile (dichlobenil) and 3,3'-iminodipropionitrile (IDPN) has been well documented. Whether there is an olfactory deflicit associted with the partial loss of the olfactory mucosa (localized around the dorsal medial meatus of the nasal cavity) has yet to be determined. Dichlobenil (100 mg/kg) or IDPN (200 mg/kg) was administered ip to adult male Long-evans rats previously trained in an olfactory task to find a food pellet buried in approximately 7.5 cm of beding in a 0.61x1.2x0.61-m Plexiglass chamber. As a positive control, another group received 300 mg/kg ip of 1-methyl-2-mercaptoimidazole (methimazole), a dosing regimen which destroys nearly all of the olfactory mucosa. All three compounds caused a transient increase in the mean latency to find the pellet, with the magnitude of the effect positively correlated with the extent of the olfactory lesion. In order to determine whether theses deficits resulted from olfactory dysfunction or impaired cognitive function (a deficit previously attributed to IDPN exposure), another group of rats was dosed as above and tested in another spatial memory task, the Morris water maze (MWM), which is less dependent upon olfactory function. No performance deficit was detected in the MWM. These data suggest the transient olfactory deficit in the dichlobenil-, IDPN-, and methimazole-treated rats is attributable to defective olfactory function.