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Lactosamine differentially affects olfactory sensory neuron projections to the olfactory bulb
Author(s) -
Schwarting Gerald A.,
Henion Timothy R.
Publication year - 2007
Publication title -
developmental neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.716
H-Index - 129
eISSN - 1932-846X
pISSN - 1932-8451
DOI - 10.1002/dneu.20536
Subject(s) - biology , olfactory bulb , neuroscience , sensory system , mutant , axon , population , olfactory system , microbiology and biotechnology , endocrinology , medicine , central nervous system , genetics , gene , demography , sociology
During embryonic development, olfactory sensory neurons extend axons that form synapses with the dendrites of projection neurons in glomeruli of the olfactory bulb (OB). The glycosyltransferase β3GnT1 regulates the expression of 1B2‐reactive lactosamine glycans that are mosaically distributed among glomeruli. In newborn β3GnT1 −/− mice, lactosamine expression is lost, and many glomeruli fail to form. To determine the role of lactosamine in OB targeting, we analyzed the trajectories of specific OR axon populations and their reactivity with 1B2 in β3GnT1 −/− mice. mI7 axons and P2 axons, both of which are weakly 1B2 + in wild‐type mice, fail to grow to their normal positions in the glomerular layer during early postnatal development and never recover in adult mutant mice. In contrast, many M72 axons, which are always lactosamine negative in wild‐type mice, survive but are misguided to the extreme anterior OB in neonatal mutant mice and persist as heterotypic glomeruli, even in adult null mice. These results show that the loss of lactosamine differentially affects each OR population. Those that lose their normal expression of lactosamine fail to form stable connections with mitral and tufted cells in the OB, disappear during early postnatal development, and do not recover in adults. Neurons that are normally lactosamine negative, survive early postnatal degeneration in β3GnT1 −/− mice but extend axons that converge on inappropriate targets in the mutant OB. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007.