The vomeronasal organ (VNO) in the nasal cavity provides chemical sensory information
to guide animal’s innate social and reproductive behaviors as well as predator and
prey interactions. The access of stimulus fluids to the VNO relies on vasomotor movement
of the vomeronasal cavernous vessels, which are controlled by the autonomic nervous
system. Little is known about whether and how chemical constituents in the stimulus
fluids are monitored to regulate their access. Using immunolabeling and transgenic
mice, we identified a dense population of solitary chemosensory cells (SCCs) at the
vomerosasal entry duct. These SCCs are trigeminally innervated, express transient
receptor potential channel M5 (TRPM5) and phospholipase C (PLC) signaling pathway.
Additionally, the SCCs express choline acetyltransferase (ChAT) and vesicular acetylcholine
transporter (VAChT) for synthesizing and packaging acetylcholine. In single-cell Ca2+imaging experiments, SCCs respond to various chemicals including bitter-tasting compounds
and odorous irritants primarily via the PLC pathway. To investigate further the role
of SCCs in regulating VNO stimulus access, we developed a quantitative dye assay to
determine the amount of stimulus fluid entering the VNO in freely behaving mice. We
found that in wild type mice, the amount of the fluid entered is inversely correlated
to the concentration of irritants and bitter substances in the fluid. In TRPM5 knockout
mice, significantly larger amounts of bitter compounds enter the VNOs, showing impaired
regulation of stimulus access. Moreover, two-week exposure to a bacterial toxicant
results in defect predator odor-evoked fear reaction in TRPM5 knockout, but not in
the wild type animals. Taken together, our data uncovered the essential role of SCCs
in regulating vomeronasal vasomotor movement, hence stimulus access to the VNO. Our
results also provide new insight into the emerging role of SCCs in chemoreception
and regulation of physiological actions.
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Publication history
Received:
May 15,
2013
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Copyright
© 2013 Published by Elsevier Inc.