Abstracts - Association for Chemoreception Sciences
Abstracts - Association for Chemoreception Sciences
Abstracts - Association for Chemoreception Sciences
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P O S T E R S<br />
#P207 POSTER SESSION IV: CHEMOSENSORY<br />
TRANSDUCTION AND SIGNALING<br />
Pannexin-1 and Connexin-43 Immunoreactivity in Rodent<br />
Taste Buds<br />
Ruibiao Yang 1,2 , Amanda Bond 1,2 , Stacey Thomas 1,2 ,<br />
John Kinnamon 1,2<br />
1<br />
Department of Biological <strong>Sciences</strong>, University of Denver<br />
Denver, CO, USA, 2 Rocky Mountain Taste & Smell Center<br />
Aurora, CO, USA<br />
Pannexin and/or connexin hemichannels may be located at sites of<br />
ATP release from rodent taste cells. We hypothesize that Type II<br />
and possibly Type III cells release ATP at sites containing<br />
pannexin and connexin hemichannels. Pannexin-1: Our data<br />
indicate that Pannexin-1-like immunoreactivity (LIR) is present in<br />
a large subset of taste cells in rodent taste buds. Pannexin-1-LIR<br />
colocalizes with PLCb2 and a-gustducin-LIR in a subset of taste<br />
cells. Some taste cells, however, display only Pannexin-1, PLCb2,<br />
or a-gustducin-LIR. A subset of TRPM-5-GFP taste cells display<br />
Pannexin-1-LIR and some taste cells express only Pannexin-1-<br />
LIR. We believe that Pannexin-1-LIR is expressed primarily in<br />
Type II cells. Pannexin-1-LIR, however, is present in a small<br />
subset of NCAM-, syntaxin-, and/or 5-HT-LIR cells. Thus, a<br />
subset of Type III taste cells exhibit Pannexin-1-LIR. Connexin-<br />
43: Connexin-43 is the most studied gap junction protein and is<br />
present in a large subset of taste cells. Connexin-43-LIR cells are<br />
spindle-shaped with large nuclei and are most likely Type II cells.<br />
Connexin-43-LIR colocalizes with TRPM5-GFP and IP3R3-LIR<br />
in subsets of taste cells. Connexin-43-LIR colocalizes with a large<br />
subset of Pannexin-1-LIR taste cells. Based on our preliminary<br />
data, most Connexin-43-LIR is believed to be present in Type II<br />
taste cells. Although a subset of Type III cells displays<br />
immunoreactivity to pannexin-1, we did not observe any<br />
colocalization between connexin-43 and the Type III cell marker,<br />
5-HT. Acknowledgements: This work is supported by NIH<br />
grants DC00285 and DC007495<br />
#P208 POSTER SESSION IV: CHEMOSENSORY<br />
TRANSDUCTION AND SIGNALING<br />
Potential modulatory effects of serotonin in taste receptor<br />
cell excitability<br />
Fang-li Zhao, Scott Herness<br />
The Ohio State University Columbus, OH, USA<br />
Serotonin (5HT) and the 5HT1A receptor subtype are thought to<br />
play an important role in the processing of gustatory in<strong>for</strong>mation<br />
via cell-to-cell communication among individual cells of the taste<br />
bud. Activation of the 5HT1A receptor is known to inhibit a<br />
number of ionic currents in taste receptor cells; additionally, 5HT<br />
inhibits ATP release from type II cells. Here we attempt to<br />
address the potential modulation locus of 5-HT on rat taste<br />
receptor cell transduction cascades using patch-clamp technique.<br />
In the gap-free recording mode, 5-HT did not affect the sustained<br />
currents with holding potentials of -50, -20, -10, and 0 mV,<br />
respectively (n = 26). This implies 5HT has no significant effect<br />
on resting state but rather modulates the active state of the cell.<br />
We further investigated the potential influence of 5HT on PIP2<br />
since this phospholipid is central to many taste transduction<br />
cascades and its resynthesis important <strong>for</strong> maintaining cellular<br />
excitability. Using an electrophysiological assay with m-3M3FBS<br />
treatment (a PLC activator) that monitors PIP2 resynthesis, we<br />
observed that 5HT as well as the 5HT1A agonist 8-OH-DPAT<br />
both were effective in preventing resynthesis of PIP2 produced<br />
by tastant stimulation (cycloheximide n = 32, and SC45647,<br />
n = 30). The effect showed strong adaptation. Further this effect<br />
was reduced with GDP-bS in recording pipette (n = 24),<br />
consistent with a G-protein dependent activation of the 5HT1A<br />
receptor. We suggest that 5-HT negatively couples with PIP2<br />
resynthesis whether during tastant challenge or post stimulus<br />
recovery. Further, since PIP2 resynthesis is necessary to restore<br />
activation on many ion channels, including hemichannels, this<br />
action may provide a mechanism <strong>for</strong> 5HT suppression of ATP<br />
release from taste receptor cells. Acknowledgements: NIH<br />
NIDCD R01 DC00401<br />
#P209 POSTER SESSION V:<br />
CENTRAL OLFACTION; CHEMOSENSORY<br />
PSYCHOPHYSICS & CLINICAL STUDIES<br />
Co-stimulation with an olfactory stimulus enhances arousal<br />
responses to trigeminal stimulation during sleep in humans<br />
Boris A. Stuck, Franziska Lenz, Jann Baja, Clemens Heiser<br />
Department of Otorhinolaryngology, Head and Neck Surgery<br />
Mannheim, Germany<br />
Recent studies have demonstrated that olfactory stimulation does<br />
not lead to arousals or awakenings during sleep. In contrast, nasal<br />
trigeminal stimulation induces dose-dependent arousal responses<br />
comparable to nociceptive stimuli. The interaction of the<br />
olfactory and trigeminal system has been demonstrated<br />
previously. The aim of the study was to investigate whether<br />
olfactory stimulation influences arousal responses to nasal<br />
trigeminal stimulation. Five normosmic volunteers were included<br />
in the trial and 10 nights of testing were per<strong>for</strong>med. Intranasal<br />
chemosensory stimulation was based on air-dilution olfactometry.<br />
For trigeminal stimulation 40% v/v CO2 was administered either<br />
with or without simultaneous stimulation with the pure olfactory<br />
stimulant H2S (8 ppm). Stimulus duration was 1s. Arousal<br />
reactions were assessed according to appearance and latency<br />
during overnight polysomnography in a period of 30 seconds<br />
after every stimulus. 200 stimulations were per<strong>for</strong>med on average<br />
per subject. Compared to isolated trigeminal stimulation,<br />
co-stimulation with H2S showed an increase in arousal frequency<br />
and a reduction in arousal latency. Arousal frequency was 12.1%<br />
without and 16.6% with olfactory co-stimulation with the<br />
strongest effect seen during light sleep (with: 32.8%, without:<br />
24%). Mean arousal latency was reduced from 5.7s without to<br />
4.4s with olfactory co-stimulation. The present results<br />
demonstrate that olfactory stimulation, although not leading to<br />
arousal during sleep, influences the frequency and latency of<br />
arousals induced by nasal trigeminal stimulation. As arousals are<br />
mostly induced by the thalamus the interaction between the two<br />
systems does not occur on a cortical but on a peripheral or early<br />
level of central processing. Acknowledgements: The study was<br />
supported by the German Research Foundation (DFG)<br />
96 | AChemS <strong>Abstracts</strong> 2010 <strong>Abstracts</strong> are printed as submitted by the author(s)