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J Neurophysiol 94: 3719-3729, 2005. First published August 17, 2005; doi:10.1152/jn.00700.2005
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Neural Representation of Bitter Taste in the Nucleus of the Solitary Tract

Christian H. Lemon and David V. Smith

Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, Tennessee

Submitted 5 July 2005; accepted in final form 15 August 2005

Based on the molecular findings that many bitter taste receptors (T2Rs) are expressed within the same receptor cells, it has been proposed that bitter taste is encoded by the activation of discrete neural elements. Here we examined how a variety of bitter stimuli are represented by neural activity in central gustatory neurons. Taste responses (spikes/s) evoked by bathing the tongue and palate with intensity-matched concentrations (in M) of 2 sugars (0.32 sucrose and 0.5 D-fructose), ethanol (40%), 4 salts (0.01 NaCl, 0.008 NaNO3, 0.01 MgCl2, and 0.05 KCl), 2 acids (0.003 HCl and 0.005 citric acid), and 10 bitter ligands (0.007 quinine-HCl, 0.015 denatonium benzoate, 0.003 L-cysteine, 0.001 nicotine, 0.005 strychnine-HCl, 0.04 tetraethylammonium chloride, 0.03 atropine-SO4, 0.005 brucine-SO4, 0.03 papaverine-HCl, and 0.009 sparteine) were recorded from 51 neurons in the nucleus of the solitary tract of anesthetized rats. Cluster analysis was used to categorize neurons into types based on responses to sucrose, NaCl, HCl, and quinine-HCl. Three groupings emerged: type S (responded optimally to sweets), type N (sodium-optimal), and type H/Q (responded robustly to bitters, acids, and salts). Multivariate analyses revealed that across-neuron patterns of response among bitter stimuli were strongly correlated. However, neural type H/Q, which was most responsive to bitter tastants, was not differentially sensitive to bitter stimuli and Na+ salts, which rats perceive as distinct. Thus central neurons most responsive to bitter substances receive significant input from receptors that mediate other tastes, indicating that bitter stimuli are not represented by activity in specifically tuned neurons.


Address for reprint requests and other correspondence: D. V. Smith, Dept. of Anatomy and Neurobiology, University of Tennessee Health Science Center, 855 Monroe Ave., Suite 515, Memphis, TN 38163 (E-mail: dvsmith{at}utmem.edu)




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