Functional impairment of the primary nociceptive analyser in the course of transganglionic degenerative atrophy.
Latency to the hind-paw lick in the hot-plate test (54 degrees C) is significantly increased (P less than 0.001) in the course of transganglionic degenerative atrophy of central terminals of primary sensory neurons. This was induced by a 30 min perineural application of 10(-8) mol Formyl-Leurosin, which results in the blockade of retrograde axoplasmic transport without Wallerian degeneration of the peripheral nerve. Values of latency return to normal in the course of synaptoneogenetic restoration of neuronal connectivity in the upper dorsal horn. The results are compatible with the working hypothesis that the beneficial effect of chronic pain therapy with Vinca alkaloid iontophoresis might be due to the fact that transganglionic degenerative atrophy is followed by the establishment of a sound, normal wiring in the upper dorsal horn in the course of restorative synaptoneogenesis.
D000135:Acid Phosphatase / Q000378:metabolism*; D000818:Animals; D001284:Atrophy; D001370:Axonal Transport / Q000187:drug effects; D005260:Female; D005727:Ganglia, Spinal / Q000473:pathology*; D009410:Nerve Degeneration; D009475:Neurons, Afferent / Q000187:drug effects*; D010146:Pain / Q000188:drug therapy; D051381:Rats; D011930:Reaction Time; D012584:Sciatic Nerve / Q000187:drug effects*; D013116:Spinal Cord / Q000187:drug effects*; D013376:Substantia Gelatinosa / Q000187:drug effects*; D014747:Vinblastine / Q000494:pharmacology*; D014748:Vinca Alkaloids / Q000494:pharmacology* / Q000627:therapeutic use; D014750:Vincristine / Q000494:pharmacology*
D014748:Vinca Alkaloids; C016463:formyl-leurosine; D014750:Vincristine; D014747:Vinblastine; D000135:Acid Phosphatase