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Olfactory Receptors: Location and Structure01:03

Olfactory Receptors: Location and Structure

The process of olfaction, also known as the sense of smell, is a sophisticated chemical response system. The specialized sensory neurons that facilitate this process, known as olfactory receptor neurons, are situated in an upper segment of the nasal cavity, known as the olfactory epithelium. Olfactory sensory neurons are bipolar, with their dendrites extending from the epithelium's apex into the mucus that lines the nasal cavity. Airborne molecules, when inhaled, traverse the olfactory...

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β3GnT2 null mice exhibit defective accessory olfactory bulb innervation.

Timothy R Henion1, Pasil A Madany, Ashley A Faden

  • 1Department of Cell Biology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA. timothy.henion@umassmed.edu

Molecular and Cellular Neurosciences
|September 26, 2012
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Summary

The glycosyltransferase β3GnT2 is crucial for vomeronasal sensory neuron (VSN) axon guidance and accessory olfactory bulb (AOB) organization. Its absence disrupts axon targeting and glomerular formation, impacting pheromone signal processing.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Developmental Biology

Background:

  • Vomeronasal sensory neurons (VSNs) project to the accessory olfactory bulb (AOB), segregating into anterior (aAOB) and posterior (pAOB) compartments to relay pheromone signals.
  • The glycosyltransferase β3GnT2 in the olfactory epithelium (OE) is known to regulate axon guidance cues for proper neuronal organization.
  • Mechanisms governing mammalian vomeronasal targeting and AOB organization are not fully understood.

Purpose of the Study:

  • To investigate the role of β3GnT2 in vomeronasal system axon guidance and AOB organization.
  • To determine how β3GnT2 influences the expression of guidance and adhesion molecules in the vomeronasal system.
  • To elucidate the impact of β3GnT2 deficiency on VSN projection patterns and glomerular formation in the AOB.

Main Methods:

  • Analysis of β3GnT2 knockout mice (β3GnT2(-/-)) and wildtype littermates.
  • Immunohistochemical staining to examine the expression patterns of ephrinA5, V2r1b, Kirrel2, and OCAM.
  • Microscopic analysis of AOB structure, including glomerular morphology and compartmentalization.

Main Results:

  • β3GnT2 deficiency alters ephrinA5 expression, leading to its upregulation on aAOB axons.
  • Despite altered ephrinA5, apical and basal VSN projections remain segregated, but V2r1b axons inappropriately innervate the aAOB due to ectopic receptor expression.
  • Loss of Kirrel2 and OCAM in β3GnT2(-/-) aAOB results in increased V2r1b glomeruli and failed formation of distinct anterior glomeruli.

Conclusions:

  • β3GnT2 plays a distinct role in the vomeronasal system, regulating guidance and adhesion molecules essential for AOB organization.
  • β3GnT2 glycosylation is vital for maintaining expression of layer-specific vomeronasal receptors and adhesion molecules.
  • Proper AOB glomerular formation and vomeronasal sensory processing depend on β3GnT2-mediated regulation of molecular expression.