Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.
Multiple mechanisms contribute to myenteric plexus ablation induced by benzalkonium chloride in the guinea-pig ileum.
Cell Tissue Res. 1997 Aug;289(2):253-64. Unique Identifier : AIDSLINE MED/97361995 Parr EJ; Sharkey KA; Neuroscience Research Group, Department of Physiology and Biophysics,; The University of Calgary, 3330 Hospital Drive N.W., Calgary, Alberta,; Canada T2N 4N1.
Abstract:
Ablation of rat myenteric plexus with benzalkonium chloride has provided a model of intestinal aganglionosis, but the degenerative responses are not well understood. We examined the effects of this detergent on neurons and glia, including expression of c-Myc, c-Jun, JunB, and c-Fos, and on immunocytes in the guinea-pig ileum. Benzalkonium chloride (0.1%) or saline was applied to the serosal surface of distal ileum. Tissues were analyzed 2, 3, or 7 days later and compared with cyclosporine-treated and untreated animals. More than 90% of myenteric neurons were destroyed in ileal segments 3-7 days after benzalkonium-chloride treatment. Glia withdrew processes from around neurons after 2 days and were mostly gone after 3 days. Neuronal c-Myc began to disappear while c-Fos, c-Jun, and JunB were evident in some neuronal nuclei after 2 or 3 days. After 3 days, widespread apoptosis was evident in the myenteric plexus. Populations of T cells, B cells, and macrophage-like cells in untreated and saline-treated myenteric plexuses were substantially increased 3 and 7 days after benzalkonium-chloride treatment. Cyclosporine delayed significant neuronal loss. We conclude that a variety of degenerative mechanisms may be active in this model, including an immune response which may actively contribute to tissue destruction.
Keywords: *Benzalkonium Compounds/PHARMACOLOGY *Detergents/PHARMACOLOGY *Ileum/DRUG EFFECTS *Myenteric Plexus/DRUG EFFECTS 971130
M97B0530
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