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      Functional and fine structural characteristics of the sensory neuron blocking effect of capsaicin.

      Naunyn-Schmiedeberg's Archives of Pharmacology
      Analgesia, Animals, Axons, ultrastructure, Capsaicin, antagonists & inhibitors, pharmacology, Chemoreceptor Cells, drug effects, Colchicine, Cornea, innervation, Cycloheximide, Cytoplasmic Granules, Dactinomycin, Fatty Acids, Unsaturated, Guinea Pigs, Mitochondrial Swelling, Nerve Endings, Nerve Tissue Proteins, biosynthesis, Neurons, RNA, Rats, Schwann Cells, Vinblastine

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          Abstract

          In the eye of rats the long-lasting specific desensitization induced by local or systemic capsaicin treatment is characterized by three phases: 1. complete insensitivity, 2. decreased sensitivity and a tendency to rapid adaptation, 3. normal initial sensitivity with a tendency to rapid adaptation to chemical pain stimuli. A low density of nicrovesicles and swollen mitochondria were found after local capsaicin treatment in certain nerve endings of the cornea of rats, but no signs of axonal degeneration or alteration in fine structure of non-neural elements were seen. Systemic capsaicin desensitization induced selective mitochondrial swelling in B type of neurons of the trigeminal ganglion which was demonstrable even 60 days after the pretreatment. Actinomycin-D, 8-azaguanine, 6-azauracil, aminopterin, mannomustin or cycloheximide in high doses did not alter the desensitizing effect of systemic capsaicin treatment. However, pretreatment of rats with colchicine or vinblastine prolonged the desensitizing effect of local capsaicin application, probably by inhibiting the axonal flow. It is concluded that capsaicin is a specific sensory neuron blocking agent having a practically irreversible effect in rats and guinea-pigs.

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