title: The regeneration of P2 olfactory sensory neurons is selectively impaired following methyl bromide lesion.
abstract: The capacity of the peripheral olfactory system to recover after injury has not been thoroughly explored. P2-IRES-tauLacZ mice were exposed to methyl bromide, which causes epithelial damage and kills 90% of the P2 neurons. With subsequent neuronal regeneration, P2 neurons recover within their usual territory to equal control numbers by 1 month but then decline sharply to roughly 40% of control by 3 months. At this time, the P2 projection onto the olfactory bulb is erroneous in several respects. Instead of converging onto 1 or 2 glomeruli per surface, small collections of P2 axons innervate multiple glomeruli at roughly the same position in the bulb as in controls. Within these glomeruli, the P2 axons are aggregated near the edge, whereas the remainder of the glomerulus contains olfactory marker protein (+), non-P2 axons, violating the one receptor-one glomerulus rule normally observed. The aggregates are denser than found in control P2-innervated glomeruli, suggesting that the P2 axons may not be synaptically connected. Based on published literature and other data, we hypothesize that P2 neurons lose out in an activity-based competition for synaptic territory within the glomeruli and are not maintained at control numbers due to a lack of trophic support from the bulb.
authors: Department of Otology and Laryngology, Harvard Medical School and Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, MA 02114, USA, Department of Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA.
authors: Eric H
authors: EH
authors: Holbrook
authors: Department of Cell and Developmental Biology and Program in Neuroscience, SUNY Upstate Medical University, 766 Irving Avenue, Syracuse, NY 13210, USA and.
authors: Carrie L
authors: CL
authors: Iwema
authors: Program in Cell, Molecular, and Developmental Biology, Sackler School of Graduate Biomedical Sciences, Tufts University, 136 Harrison Avenue, Boston, MA 02111, USA.
authors: Carolyn E
authors: CE
authors: Peluso
authors: Department of Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA, Department of Cell and Developmental Biology and Program in Neuroscience, SUNY Upstate Medical University, 766 Irving Avenue, Syracuse, NY 13210, USA and jim.schwob@tufts.edu.
authors: James E
authors: JE
authors: Schwob
mesh_terms: D000818:Animals; D006842:Hydrocarbons, Brominated / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D051379:Mice; D020297:Mice, Congenic; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009831:Olfactory Mucosa / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D011984:Sensory Receptor Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*
chemical_list: D006842:Hydrocarbons, Brominated; C005218:methyl bromide
keywords: axonal regeneration; olfactory bulb; olfactory epithelium; olfactory receptor; olfactory sensory neuron; olfactotoxin