Blockade of retrograde axoplasmic transport induces transganglionic degenerative atrophy of central terminals of primary nociceptive neurons.
If applied locally around a peripheral sensory nerve, Formyl-Leurosin, a semi-synthetic diindol alkaloid of Vinca rosea--that, just like other mitotic spindle inhibitors, induces blockade of axoplasmic transport via inhibiting microtubular function--causes transganglionic degenerative atrophy of central terminals of primary nociceptive neurons in the substantia gelatinosa Rolandi of the spinal cord. In contrast, if applied to dorsal roots, Formyl-Leurosin fails to induce such alterations. Based upon these observations it is postulated that blockade of retrograde axoplasmic transport, rather than that of the orthograde one, is the decisive factor in the pathomechanism of transganglionic degenerative atrophy.
D000818:Animals; D001284:Atrophy; D001370:Axonal Transport / Q000187:drug effects; D005260:Female; D005727:Ganglia, Spinal / Q000187:drug effects / Q000473:pathology* / Q000502:physiology; D008297:Male; D009410:Nerve Degeneration; D009619:Nociceptors / Q000473:pathology*; D051381:Rats; D012183:Retrograde Degeneration; D014748:Vinca Alkaloids / Q000494:pharmacology
D014748:Vinca Alkaloids; C016463:formyl-leurosine