Acrylamide-induced neuropathic changes in rat enteric nerves: similarities with effects of streptozotocin-diabetes.
The effect of acrylamide intoxication (a widely used model for autonomic neuropathy) on the fluorescence intensity and density of catecholamine- and peptide-containing nerve fibres and tissue content of noradrenaline and the peptides vasoactive intestinal polypeptide, calcitonin gene-related peptide, substance P and neuropeptide Y in the enteric nerves of rat ileum was examined. Histochemical and immunohistochemical techniques were used to localize catecholamine- and peptide-containing nerve fibres. The tissue content of noradrenaline was measured using high-performance liquid chromatography, and an enzyme-linked immunosorbent assay technique was used to determine the tissue content of the peptides investigated. Acrylamide intoxication caused a significant decrease in the density of catecholamine-containing nerve fibres and tissue content of noradrenaline in the myenteric plexus of rat ileum. A decrease in tissue content and immunoreactivity of calcitonin gene-related peptide and an increase in vasoactive intestinal polypeptide was seen in the myenteric plexus of ileum from acrylamide-intoxicated rats. In the submucous plexus, the acrylamide treatment caused a decrease in calcitonin gene-related peptide immunoreactivity and an increase in vasoactive intestinal polypeptide and neuropeptide Y immunoreactivity. There was no change in either tissue content or immunoreactivity of substance P in both myenteric and submucous plexuses of the treated rat ileum. These changes have a striking similarity with those found in the enteric nerves of streptozotocin-diabetic rat ileum, suggesting the possible presence of an underlying common mechanism(s) in the development of neuropathic changes in the autonomic nerves of acrylamide-intoxicated and streptozotocin-diabetic rats.
Belai
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A
Department of Anatomy and Developmental Biology, University College London, UK.
Burnstock
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G
D020106:Acrylamide; D000178:Acrylamides / Q000633:toxicity*; D000818:Animals; D017776:Autonomic Pathways / Q000737:chemistry / Q000166:cytology / Q000187:drug effects*; D015740:Calcitonin Gene-Related Peptide / Q000032:analysis; D002395:Catecholamines / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000139:chemically induced*; D007422:Intestines / Q000294:innervation; D008297:Male; D009412:Nerve Fibers / Q000187:drug effects; D009478:Neuropeptide Y / Q000032:analysis; D009638:Norepinephrine / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013373:Substance P / Q000032:analysis; D014660:Vasoactive Intestinal Peptide / Q000032:analysis
D000178:Acrylamides; D002395:Catecholamines; D009478:Neuropeptide Y; D020106:Acrylamide; D013373:Substance P; D014660:Vasoactive Intestinal Peptide; D015740:Calcitonin Gene-Related Peptide; D009638:Norepinephrine