Page 24 - ACHEMS 2012 PROGRAM

24 | AChemS Abstracts 2012 Abstracts are printed as submitted by the author(s)
#46 PLATFORM PRESENTATIONS:
TASTE
The effect of the CALHM1 gene on behavior and taste
nerve responses
Göran Hellekant1, Philippe Marambaud2, Sze Leung1,
Maria Abernathy1
1Biomedical Sciences, Medical School, University of Minnesota,
USA Duluth, MN, USA, 2Pathology, The Feinstein Institute,
Albert Einstein College of Medicine, Bronx, Duluth, NY, USA,
3Biomedical Sciences, Medical School, University of Minnesota
Duluth, MN, USA, 4Biomedical Sciences, Medical School,
University of Minnesota, Duluth, MN, USA
Type II taste receptor cell (TRC) bears either sweet receptors,
T1R2/3, or umami T1R1/3 or bitter T2Rs receptors. These
receptors constitute the first links in an intracellular cascade,
which leads to impulses in taste fibers. Important here is the finding
that sweet and bitter receptors never co-localize in the same TRC.
Studies have also shown that in the Type II TRCs a calcium
activated sodium channel, TRPM5 is important (Damak et al.
2006). In the following we studied the gustatory effects of another
calcium activated channel CALHM1. In taste its existence was first
described by (Hevezi et al. 2009) who found a high concentration
in the Type II TRCs. Here we present results of two-bottle
preference tests and electrophysiological recordings from the
chorda tympani proper nerve in mice with (WT) and without
expression of the CALHM1 gene (CALHM1 null mice). We used
ammonium chloride as standard, and as test solutions NaCl, IMP,
MSG, monocalcium di-L-glutamate, QHCl, sparteine, denatonium
benzoate, ascorbic and citric acid and six sweeteners. Our data
show that: the CALHM1 null mice don’t discriminate between
water and sweet and have an impaired ability to taste bitter,
CALHM1 null mice discriminate between salty and water or acid
and water at the same concentrations as the WT. These deficits can
be explained with an absence of a taste response in the chorda
tympani nerve to sweet and a lowered response to bitter. The
chorda tympani nerve response is not different to salty and sour
compounds in WT and CALHM1 null mice. References:
Damak S, et al. 2006. Trpm5 null mice respond to bitter, sweet,
and umami compounds. Chem Senses 31: 253-264. Hevezi P, et al..
2009. Genome-wide analysis of gene expression in primate taste
buds reveals links to diverse processes. PLoS One 4: e6395.
Acknowledgements: Medical School-Duluth, MN, USA
#47 PLATFORM PRESENTATIONS:
TASTE
Regulation of Artificial Sweetener Acceptance by Glucose
Metabolic Rate
Xueying Ren1,2, Jozelia G Ferreira1,2, Luis A Tellez1,2,
Ivan E de Araujo1,2
1The J.B. Pierce Laboratory New Haven, CT, USA,
2Department of Psychiatry, Yale University New Haven, CT, USA
The formation of preferences for sweet tastants is influenced by
both gustatory and postingestive signals. Accordingly striatal
dopamine targets, which regulate food intake, are responsive to
both classes of cues. We had previously shown that disrupting
glucose utilization with 2-deoxyglucose (2-DG) injections inhibits
dopamine release in dorsal striatum. We therefore hypothesized
that 2-DG injections would depress acceptance for non-caloric
sweeteners but would be ineffective in suppressing glucose
acceptance. We have found that one single 2-DG injection
produced a significant and long-lasting suppression in intake
levels of the artificial sweetener sucralose, but not of glucose.
We concluded that 2-DG does not affect glucose preference
because glucose, unlike artificial sweeteners, can counteract the
negative physiological effects of 2-DG. The effect did not depend
on sweet signaling since short-term preference tests show that
sucralose remained equally preferred over glucose even after
2-DG injections; in addition, ingesting sucralose concomitantly
to intragastric glucose was unaltered by 2-DG injections.
Furthermore, striatal dopamine levels were strongly suppressed
by 2-DG injections during sucralose, but not glucose, sessions.
Our findings therefore demonstrate that pairing sweeteners with
negative physiological states produce a long-lasting suppression in
the intake of sweeteners lacking energy content. More generally,
our findings indicate that artificial sweetener intake is strongly
influenced by glucose metabolism. Acknowledgements: NIDCD
Grant RO1 DC009997
#49 SYMPOSIUM: THE ROLE OF RESPIRATION IN
OLFACTORY & FLAVOR PROCESSING
Dissecting the effects of sniff variations on olfactory
bulb (OB) activity
Nathalie Buonviso
Centre de Recherche en Neurosciences de Lyon, CNRS UMR5292,
Inserm U1028, Université Lyon1 Lyon, France
In terrestrial mammals, odorant molecules sampling is inextricably
related to the respiratory dynamics. Therefore, odorant molecules
reach the olfactory epithelium with a variable concentration
depending on i) the respiratory phase, ii) the frequency and flow
rate of the successive respiratory cycles. We have been interested in
the way OB activity is modified by such variations, rather than in
the informational content of the respiration-related activity. The
question is how variations in OB input, related to respiratory
dynamics, are reflected in the OB activity? We addressed this
question using a simulated nasal airflow protocol in anesthetized rat
combined with either voltage sensitive dye imaging (VSDi) of OB
glomerular maps or electrophysiological recordings of OB LFP and
mitral/tufted cells activity. This model allowed us to impose sniff
frequency and flow rate independently or concomitantly. Both
VSDi and electrophysiological signals revealed that sniff frequency
and flow rate could act synergistically to maintain OB sniffing-
related rhythmicity even during high-frequency sniffing (10 Hz).
However, both signals show that flow rate and frequency can also
O R A L A B S T R A C T S