Abstracts - Association for Chemoreception Sciences

nerve fibers. Nasal SCCs respond to bitter compounds including
bacterially-produced molecules, to evoke protective respiratory
reflexes and early inflammatory responses (Gulbransen 2008,
Tizzano 2010 and AChemS 2012). Here we test whether SCCmediated
pro-inflammatory responses require activation of the
trigeminal nerve and subsequent peptidergic neurotransmission,
or whether SCC activation triggers local inflammation via
an intramucosal paracrine signaling mechanism. When
denatonium (10mM) is instilled into the nasal passageways,
it evokes SCC-dependent plasma leakage and local mast cell
(MC) degranulation (Tizzano AChemS 2012). Chemical
ablation of peptidergic nerve fibers with resiniferatoxin (RTX,
an ultrapotent analog of capsaicin) eliminates both denatoniummediated
plasma leakage and MC degranulation. These results
show that the peptidergic nerve fibers are necessary for these
SCC-mediated pro-inflammatory events. Moreover, injection of
L732138 (5mg/kg), an inhibitor of the neurokinin 1 (substance
P) receptor present on blood vessels, prevents denatoniuminduced
plasma leakage. This indicates that substance P is the
mediator for plasma leakage. Our results demonstrate that
activation of the SCCs leads to a rapid, local pro-inflammatory
response via neurogenic mechanisms. This fast pro-inflammatory
response, driven by the SCCs in conjunction with the trigeminal
nerve, represents a 1st line of defense against respiratory
epithelial assault by noxious chemicals and bacterial pathogens.
Acknowledgements: NIDCD R03 DC012413 (M.T.), R01
DC009820 (T.E.F.), and P30 DC04657 (to D. Restrepo)
#P124 POSTER SESSION III:
TRIGEMINAL; HUMAN OLFACTORY
PSYCHOPHYSICS; TASTE PERIPHERY
The Influence of Bubbles on the Perception of
Carbonation Bite
Paul M Wise 1 , Stephen R Thom 2 , Madeline Wolf 1 , Bruce Bryant 1
1
Monell Chemical Senses Center Philadelphia, PA, USA,
2
University of Pennsylvania/Institute for Environmental Medicine
Philadelphia, PA, USA
Although many people assume that the bite of carbonation is due
to tactile stimulation of the oral cavity by bubbles, it has become
increasingly clear that carbonation bite comes mainly from
formation of carbonic acid in the oral mucosa. In Experiment
1, we asked whether bubbles were in fact required to perceive
carbonation bite. Subjects rated oral pungency from several
concentrations of carbonated water both at normal atmospheric
pressure (at which bubbles could form) and at 2.0 atmospheres
pressure (at which bubbles did not form). Ratings of carbonation
bite under the two pressure conditions were essentially identical,
indicating that bubbles are not required for pungency. In
Experiment 2, we created controlled streams of air bubbles
around the tongue in mildly pungent CO 2
solutions to determine
how tactile stimulation from bubbles affects carbonation bite.
Since innocuous sensations like light touch and cooling often
suppress pain, we predicted that bubbles might reduce rated bite.
Contrary to prediction, air bubbles flowing around the tongue
significantly enhanced rated bite, without inducing perceived
bite in blank (un-carbonated) solutions. Accordingly, though
bubbles are clearly not required for carbonation bite, they may
well modulate perceived bite. More generally, the results show
that innocuous tactile stimulation can enhance chemogenic
pain. Possible physiological mechanisms are discussed.
Acknowledgements: Supported in part by Anheuser-Busch InBev
#P125 POSTER SESSION III:
TRIGEMINAL; HUMAN OLFACTORY
PSYCHOPHYSICS; TASTE PERIPHERY
Acid detection by TRPV1 channels in both ‘taste blind’
(P2X-KO) and C57 mice
Meghan L Bills, Jennifer M Stratford, Thomas E Finger
University of Colorado School of Medicine/Department of Cell
and Developmental Biology Aurora, CO, USA
In the oropharynx the low pH of acidic solutions is detected
via taste as sour, and by general mucosal fibers as pungency or
chemesthesis. This results in the behavioral avoidance of acidic
stimuli but the relative contribution of these two systems is
unknown. Genetic deletion of the purinergic receptors P2X2
and P2X3 (P2X-KO) results in interruption of taste bud-tonerve
transmission and consequent loss of taste responses in
the gustatory nerves. Although P2X-KO mice do not respond
behaviorally to most tastants, they continue to avoid acids at
similar concentrations as wildtypes. General mucosal afferents
express TRPV1 channels, which are activated by low pH and
may underlie this avoidance of acids. To test this, P2X-KO
(n=8) and C57 (n=12) mice were assessed using a two-bottle
preference test in which one bottle contained 20 mM citric acid
(CA) and the other water. The test was given in the presence and
absence of the TRPV1 antagonist Iodoresiniferatoxin (I-RTX).
Both strains showed a significant decrease in avoidance with
I-RTX versus vehicle (p