Free accessResearch articleFirst published online 1991-9
Morphometric Analysis of Rat Trigeminal Ganglion Cells and Their Vibrissa Follicle Nerve Axons Following Multiple Low-Dose Exposure to the Carbamate Insecticide Aldicarb
Chronic carbamate exposure is reported to cause somatosensory dysfunction in humans. The limited experimental literature on neuropathic effects of repeated, low-level carbamate exposure is equivocal and does not address effects on well-defined somatosensory pathways. In this study, adult Sprague-Dawley rats were given 0.2 mg/kg/day of aldicarb, by oral gavage, for 90–114 days. The daily dose was below that capable of inducing clinical signs of cholinergic poisoning but inhibited acetylcholinesterase in spinal cord and blood. Aldicarb was evaluated for its ability to cause death or morphologic alteration of sensory neurons innervating C1 mystacial vibrissa follicles. Light and electron microscopy were used to examine the number of myelinated axons in C1 vibrissa follicle nerves and the respective areas of these axons and their myelin sheaths. Retrograde axonal transport was used with fluorescence microscopy to examine the number and diameter of the cell bodies of C1 vibrissa follicle nerve axons. No differences were observed between aldicarb-treated and control groups for any of these dependent variables. This study indicates that repeated exposure to aldicarb, at a dose below that causing sufficient acetylcholinesterase inhibition to elicit clinical signs, does not produce an anatomic correlate for somatosensory dysfunction in rats.
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