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#P246
POSTER SESSION VI:
OLFACTION CNS; TASTE PERIPHERY &
CNS; MULTIMODAL RECEPTION
Accounting for trial-to-trial variability unmasks a sudden
transition to palatability coding in gustatory cortex
Brian F Sadacca, Tony Vladusich, Paul M Miller, Donald B Katz
Brandeis University Waltham, MA, USA
Single neurons in the rodent insular cortex respond to the delivery
of natural rewards with time-varying firing rate patterns. Distinct
epochs of these responses correlate with different stimulus
properties, with one response epoch faithfully reflecting how these
animals value each stimulus. With detailed modeling, it has become
clear that these responses are not perfectly stimulus-locked, and
some trial-to-trial variability may mask when and how strongly this
value-based coding appears in cortex. To explore this, we modeled
our cortical ensembles as sequences of ensemble rate-states through
hidden Markov modeling (HMM), and have found that by aligning
neural responses to the onset of one of these rate-states, the onset of
palatability coding in single neurons and in the population at-large
appears more suddenly and stronger than without this realignment.
Acknowledgements: This work was supported by National
Institutes of Health/National Institute on Deafness and Other
Communication Disorders Grants R01DC00945, R01DC007703,
F31DC009955, and the Swartz Foundation.
#P247
POSTER SESSION VI:
OLFACTION CNS; TASTE PERIPHERY &
CNS; MULTIMODAL RECEPTION
Neuroanatomical maps of sweet and umami taste in
the mouse PBN
Jennifer M Saputra
1
, Malinda EC Fitzgerald
1,2
, John D Boughter
1
1
University of Tennessee Health Science Center/Anatomy &
Neurobiology Memphis, TN, USA,
2
Christian Brothers
University/Department of Biology Memphis, TN, USA
Umami and sweet taste share common transduction mechanisms,
including the T1R family of taste receptors. We sought to
characterize whether or not these peripheral commonalities lead to
similar patterns of neuronal activation in the parabrachial nucleus
(PBN) of male and female C57BL/6J (B6) mice. Sweet and umami
taste stimuli, including sucrose, saccharin, monopotassium
glutamate (MPG), + inosine monophosphate (IMP), an MPG+IMP
mixture, and deionized water were administered via an intraoral
cannula in a 20 minute taste reactivity test. These tests were
videotaped, and the pattern of ingestive behavior was reviewed and
scored at a later time following testing. Two hours after the start of
behavior, mice were perfused and immunohistochemistry for the
immediate early gene protein c-Fos was performed. C-Fos positive
nuclei were mapped and quantified throughout the span of the
mouse PBN shown to possess taste-activated neurons. Generally,
each stimulus evoked c-Fos in the caudal PBN, including the
medial, waist and ventral lateral subnucleus. The sweet stimuli and
the MPG-IMP mixture also elicited robust c-Fos at an intermediate
level in the lateral area, including a dense cluster of activated
neurons in the dorsal lateral (dl) subnucleus. This close
correspondence between sweet and “synergistic” umami mixtures
supports the idea that these particular stimuli evoke a similar
perception in mice. Acknowledgements: NIH DC000353 (J.D.B.)
#P248
POSTER SESSION VI:
OLFACTION CNS; TASTE PERIPHERY &
CNS; MULTIMODAL RECEPTION
Mapping central representation of MSG taste in the nucleus of
the solitary tract using mice that lack the T1R3 receptor
subunit important for sweet and umami taste
Jennifer M. Stratford, Thomas E. Finger
Rocky Mountain Taste and Smell Center, Department of Cell and
Developmental Biology, Program in Neuroscience, University of
Colorado Denver Anschutz Medical Campus Aurora, CO, USA
The sense of taste is intimately associated with the regulation of
food intake. Yet, little is known regarding how loss of taste input
may reorganize the way taste information is represented in the
central nervous system. Particular taste qualities tend to activate
distinct subdivisions of the nucleus of the solitary tract (nTS), as
determined by patterns of c-Fos activation. For example, MSG
preferentially activates cells within medial and mid subregions of
the nucleus. Our previous study (Stratford and Finger, 2010)
showed that complete loss of taste input into the brainstem (via
genetic deletion of the P2X2/P2X3 receptor subunits) resulted in
loss of quality- specific representation within the nTS. Thus, in the
absence of taste information, orosensory representation in the nTS
is reorganized. However, whether similar brainstem reorganization
occurs following loss of specific taste modalities (e.g. sweet, salty,
bitter, sour, umami) is unknown. Therefore, our current study
measured changes in nTS coding space following a combined loss
of sweet and umami sensory input induced by deletion of the T1R3
subunit. We found that MSG-induced (a combination of Na+ and
umami) c-Fos expression was reduced in T1R3 knockout mice
(T1R3 KO) as compared to WT mice- particularly in areas we
previously identified as being glutamate-responsive. In contrast, c-
Fos patterns evoked by citric acid were similar between WT and
T1R3 KO mice. Together, these results suggest that loss of specific
taste modalities may result in a corresponding loss of central
representation within in the brainstem. Further investigation is
required in order to test whether there is a systematic remapping of
taste quality in the nTS of mice in which specific taste modalities
are genetically deleted. Acknowledgements: Supported by NIH
grants to TEF and JMS.
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