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Chem. Senses 26: 359-369, 2001
© Oxford University Press 2001

Rhinotopy is Disrupted During the Re-innervation of the Olfactory Bulb that Follows Transection of the Olfactory Nerve

Marc D. Christensen1,2, Eric H. Holbrook3,4, Richard M. Costanzo3,4 and James E. Schwob1

1 Department of Cell and Developmental Biology and 2 Department of Neurosurgery, SUNY Upstate Medical University, Syracuse, NY 13210 and 3 Department of Physiology and 4 Department of Otolaryngology–Head and Neck Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298, USA

Correspondence to be sent to: James E. Schwob, Department of Anatomy and Cellular Biology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA. e-mail: jim.schwob{at}tufts.edu

Re-innervation of the olfactory bulb was investigated after transection of the olfactory nerve using monoclonal antibody RB-8 to assess whether rhinotopy of the primary olfactory projection is restored. In normal animals RB-8 heavily stains the axons, and their terminals, that project from the ventrolateral olfactory epithelium onto glomeruli of the ventrolateral bulb (termed RB-8+). In contrast, axons from dorsomedial epithelium are unlabeled (RB-8) and normally terminate in the dorsomedial bulb. Sprague–Dawley rats underwent unilateral olfactory nerve transection and survived for 6 weeks prior to perfusion, sectioning and immunostaining with RB-8. Nerve lesion does not shift the position of the boundary between RB-8+ and RB-8 regions of the epithelium. However, following transection and bulb re-innervation, the distribution of RB-8+ and RB-8 axons is markedly abnormal. First, in all 10 experimental animals RB-8 axons displace RB-8+ axons from anterior glomeruli. Furthermore, the usual target of the RB-8 fibers, i.e. the dorsomedial bulb at more posterior levels of the bulb, remains denervated, judging by the lack of staining with antibodies that label axons derived from all epithelial zones. Finally, RB-8+ fibers invade foreign territory in the dorsolateral bulb on the lesioned side in some cases. The shifts in terminal territory in the bulb after transection contrast with the restoration of the normal zonal patterning of the projection after recovery from methyl bromide lesion, but is consistent with reports of mistargeting by a receptor-defined subset of neurons after transection.


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