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ToxSci Advance Access published online on August 9, 2007
Toxicological Sciences, doi:10.1093/toxsci/kfm213
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Published by Oxford University Press 2007.

Muscarinic Receptor Dysfunction Induced by Exposure to Low-levels of Soman Vapor

Paul A. Dabisch1, Michael S. Horsmon1, William T. Muse1, Robert J. Mioduszewski1 and Sandra Thomson1

1 Operational Toxicology Team, U.S. Army Edgewood Chemical Biological Center, Aberdeen Proving Ground, MD, USA

Address correspondence to: Paul A. Dabisch, Ph.D., Operational Toxicology Team, US Army Edgewood Chemical Biological Center, ATTN: AMSRD-ECB-RT-TT, 5183 Blackhawk Road, Aberdeen Proving Ground, MD 21010-5424, Phone: 410-436-2712, Fax: 410-436-7129, E-mail: paul.a.dabisch{at}us.army.mil

Received June 22, 2007; revision received August 2, 2007; accepted August 3, 2007


  Abstract

In the eye, it has been previously reported that exposure to a cholinesterase inhibitor results in a reduced miotic response following prolonged exposure, and a decreased miotic response to the cholinergic agonists. However, no studies exist that characterize the effect of a single low-level vapor exposure to a nerve agent on parasympathetic function in the eye, or determine the threshold dose for such an effect. The present study investigated the hypotheses that a single low-level exposure to soman vapor would result in dysfunction of the parasympathetic pathway mediating the pupillary light reflex resulting from a loss of muscarinic receptor function on the pupillary sphincter muscle Adult male rats were exposed to soman vapor in a whole-body dynamic airflow exposure chamber. Rats exposed to low levels of soman vapor dose-dependently developed miosis (threshold dose between 4.1 and 6.1 mg-min/m3). Pupil size returned to pre-exposure levels within 48 hours due to desensitization of pupillary muscarinic receptors, as assessed by the pupillary response to the muscarinic agonist oxotremorine. An attenuated pupillary light reflex was also present in miotic animals (threshold dose near 6.1 mg-min/m3). While pupil size recovers within 48 hours, other measures of pupillary function, including the light reflex, acetylcholinesterase activity, and muscarinic receptor responsiveness, did not return to normal for up to 10 days post exposure. Recovery of the light reflex coincided with the recovery of pupillary muscarinic receptor function, suggesting that the attenuation of the light reflex was due to receptor desensitization.


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