title: Effects of neonatal axoplasmic transport attenuation on the response properties of vibrissae-sensitive neurons in the trigeminal principal sensory nucleus of the rat.
abstract: We have previously shown that attenuation of axoplasmic transport by application of vinblastine to the developing infraorbital nerve (ION) results in a loss of central vibrissae-related patterns that is not accompanied by changes in the receptive field sizes for the V primary afferents innervating the whisker follicles. The present study examines the relationship between the loss of central vibrissae-related patterns and alterations in the response properties of neurons in the V principal sensory nucleus (PrV) of adult rats that sustained application of vinblastine to the ION at birth. Absence of histochemically demonstrable vibrissae-related patterns in PrV resulted in only modest changes in the receptive fields and response properties of vibrissae-sensitive neurons in this nucleus that projected to the contralateral thalamus. Response latencies to electrical activation of the V ganglion were similar in treated and untreated animals. The mean receptive field size was significantly increased from 1.3 +/- 0.7 vibrissae in controls to 1.7 +/- 0.9 vibrissae in vinblastine-treated animals, and the percentage of cells yielding a tonic response to vibrissae deflection was markedly reduced (p < 0.01 for both measures). Phasically responding cells recorded in vinblastine-treated animals showed a significant reduction in the mean number of spikes per stimulus following deflection of the vibrissae in either the preferred or non-preferred direction relative to cells recorded in normal animals (p < 0.05). The present results indicate that disruption of the normal vibrissae-related aggregates of neurons in PrV by application of vinblastine to the ION has limited effects on the functional representation of the vibrissae in this nucleus.
authors.affiliation: Department of Anatomy and Neurobiology, Medical College of Ohio, Toledo 43614-5804, USA.
authors.forename: N L
authors.initials: NL
authors.lastname: Chiaia
authors.forename: S
authors.initials: S
authors.lastname: Zhang
authors.forename: R S
authors.initials: RS
authors.lastname: Crissman
authors.forename: R W
authors.initials: RW
authors.lastname: Rhoades
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D000972:Antineoplastic Agents, Phytogenic; D001370:Axonal Transport / Q000502:physiology*; D003714:Denervation; D004594:Electrophysiology; D009475:Neurons, Afferent / Q000502:physiology*; D010812:Physical Stimulation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000502:physiology; D014110:Touch / Q000502:physiology; D014278:Trigeminal Nuclei / Q000166:cytology / Q000502:physiology*; D014738:Vibrissae / Q000294:innervation* / Q000502:physiology; D014750:Vincristine
chemical_list: D000972:Antineoplastic Agents, Phytogenic; D014750:Vincristine