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Development. 2015 Dec 15;142(24):4318-28. doi: 10.1242/dev.123943. Epub 2015 Nov 2.

Tag1 deficiency results in olfactory dysfunction through impaired migration of mitral cells.

Author information

1
Department of Basic Science, Faculty of Medicine, University of Crete and Institute of Molecular Biology and Biotechnology-FoRTH, Vassilika Vouton, Heraklion, Crete 71110, Greece.
2
Department of Basic Science, Faculty of Medicine, University of Crete and Institute of Molecular Biology and Biotechnology-FoRTH, Vassilika Vouton, Heraklion, Crete 71110, Greece msavaki@imbb.forth.gr karagoge@imbb.forth.gr.
3
Laboratory of Biology, Faculty of Nursing, School of Health Sciences, University of Athens, Papadiamantopoulou 123, Athens GR11527, Greece.

Abstract

The olfactory system provides mammals with the abilities to investigate, communicate and interact with their environment. These functions are achieved through a finely organized circuit starting from the nasal cavity, passing through the olfactory bulb and ending in various cortical areas. We show that the absence of transient axonal glycoprotein-1 (Tag1)/contactin-2 (Cntn2) in mice results in a significant and selective defect in the number of the main projection neurons in the olfactory bulb, namely the mitral cells. A subpopulation of these projection neurons is reduced in Tag1-deficient mice as a result of impaired migration. We demonstrate that the detected alterations in the number of mitral cells are well correlated with diminished odor discrimination ability and social long-term memory formation. Reduced neuronal activation in the olfactory bulb and the corresponding olfactory cortex suggest that Tag1 is crucial for the olfactory circuit formation in mice. Our results underpin the significance of a numerical defect in the mitral cell layer in the processing and integration of odorant information and subsequently in animal behavior.

KEYWORDS:

Migration; Mitral cells; Olfaction

PMID:
26525675
DOI:
10.1242/dev.123943
[Indexed for MEDLINE]
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