title: Effects of neonatal attenuation of axoplasmic flow or transection of the rat's infraorbital nerve on the morphology of individual trigeminal primary afferent terminals in the brainstem.
abstract: Attenuation of axoplasmic transport in the infraorbital nerve (ION), or transection of this trigeminal (V) branch at birth, results in degradation of the central cellular aggregates related to the mystacial vibrissae. However, blockade of axoplasmic transport does not result in the nearly 90% loss of ION ganglion cells that follows neonatal transection of this nerve. The present study was undertaken to further characterize the response of individual ION axons to attenuation of axoplasmic transport and to compare these effects to the changes observed following nerve transection. Neurobiotin injections were made into the V ganglion on postnatal day (P-) 6 in normal rats and animals that had vinblastine applied to the ION or received transection of the ION on P-0. Individual labeled fibers in the portions of V nucleus principalis (PrV) and subnucleus interpolaris (SpI) innervated by the ION were drawn from single sections with the aid of a computer. Morphological analysis of fibers drawn in SpI indicated no significant differences between axons from normal and vinblastine-treated animals. The fibers drawn from rats that sustained ION transection had significantly more branch points (P < 0.05) than those from either normal or vinblastine-treated animals. In PrV, fibers drawn from vinblastine-treated rats had a slightly, but significantly, larger total process length and cross-sectional area than those from the normal animals (P < 0.05). There were no other significant differences among the three groups of axons. These results support the conclusion that application of vinblastine to the developing ION does not dramatically alter the morphologic patterning of the central arbors of its axons.
mesh_terms: D000344:Afferent Pathways / Q000473:pathology; D000818:Animals; D000831:Animals, Newborn; D001370:Axonal Transport / Q000187:drug effects*; D001369:Axons / Q000187:drug effects / Q000648:ultrastructure; D019771:Axotomy; D001710:Biotin / Q000031:analogs & derivatives; D002452:Cell Count; D003078:Colchicine / Q000633:toxicity; D009411:Nerve Endings / Q000648:ultrastructure*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012668:Trigeminal Ganglion / Q000473:pathology; D014276:Trigeminal Nerve / Q000473:pathology; D061221:Trigeminal Nerve Injuries; D014278:Trigeminal Nuclei / Q000473:pathology*; D014738:Vibrissae / Q000294:innervation*; D014747:Vinblastine / Q000633:toxicity