Depletion of substance P and somatostatin in the upper dorsal horn after blockade of axoplasmic transport.
In the upper dorsal horn of the rat lumbosacral spinal cord, substance P and somatostatin are present in two distinct and different populations of primary central afferent terminals. Substance-P-positive terminals are mainly concentrated in lamina I, while somatostatin-positive terminals are confined to lamina II. Although these two populations of primary afferent terminals differ at light- and electron-microscopic level, they are equally affected by transganglionic degenerative atrophy (TDA) which is induced by the blockade of axoplasmic transport in the segmentally related, ipsilateral sensory nerve by the local application of Vinblastin, a microtubule inhibitor. In consequence, substance P and somatostatin are depleted in the medial and intermediate portions of the upper dorsal horn, while the lateralmost area, which represents the postaxial portion of the dermatome, remains virtually intact. Substance P and somatostatin in propriospinal elements and the axonal meshwork within the dorsolateral funicle are not affected by TDA. Neurotensine, a propriospinal neuropeptide, does not show any alterations in the affected spinal segments.
D000818:Animals; D001370:Axonal Transport / Q000187:drug effects; D005260:Female; D006651:Histocytochemistry; D008297:Male; D008854:Microscopy, Electron; D009496:Neurotensin / Q000378:metabolism; D051381:Rats; D013004:Somatostatin / Q000378:metabolism*; D013116:Spinal Cord / Q000378:metabolism* / Q000648:ultrastructure; D013373:Substance P / Q000378:metabolism*; D014747:Vinblastine / Q000494:pharmacology
D013373:Substance P; D009496:Neurotensin; D013004:Somatostatin; D014747:Vinblastine