Perception of sweet taste is important for voluntary alcohol consumption in mice

Blednov, Yuri A.; Walker, Danielle; Martinez, Maria M.; Levine, Macy I.; Damak, Sami; Margolskee, Robert F.

doi:10.1111/j.1601-183x.2007.00309.x

Cited by 70 publications

(60 citation statements)

References 76 publications

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“…It is suggested that the ability of ethanol to stimulate neural pathways involved in the transduction of sweet taste (Hellekant et al 1997;Lemon et al 2004) plays an important role in its consumption (Blednov et al 2008). Consistent with this, genetic deletion of T1R3 and its associated G protein subunit (␣-gustducin) or the downstream nonspecific cation channel (TRPM5) significantly decreases alcohol preference in KO mice (Ellingson et al 2009).…”

Section: Alcohol Preference and Sweet Tastementioning

confidence: 81%

“…Differences in sensitivity to or preference for salty taste have been reported in subjects with a paternal history of alcohol dependence relative to control subjects with no paternal history (Scinska et al 2001). A positive association exists between ethanol intake and sweet taste (Stewart et al 1994;Woods et al 2003) involving the gene for T1R3 (Bachmanov et al 2001(Bachmanov et al , 2002Blednov and Harris 2007;Blednov et al 2008;Blizard 2007;Brasser et al 2010;Inoue et al 2004;Lu et al 2005;Nelson et al 2001), a G protein-coupled receptor (GPCR) that combines with another GPCR (T1R2) to function as the broadly tuned, heterodimeric, sweet taste receptor T1R2ϩT1R3 Zhao et al 2003). Alcohol dependence and use also show significant association with the T2R38 gene, a marker for 6-n-propylthiouracil bitterness, and with hT2R16, a gene encoding a taste receptor for the bitter-tasting ␤-glucopyranosides (Duffy et al 2004;Hinrichs et al 2006).…”

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confidence: 99%

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Strain differences in the neural, behavioral, and molecular correlates of sweet and salty taste in naive, ethanol- and sucrose-exposed P and NP rats

Coleman¹,

Williams²,

Phan³

et al. 2011

Journal of Neurophysiology

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Strain differences between naive, sucrose- and ethanol-exposed alcohol-preferring (P) and alcohol-nonpreferring (NP) rats were investigated in their consumption of ethanol, sucrose, and NaCl; chorda tympani (CT) nerve responses to sweet and salty stimuli; and gene expression in the anterior tongue of T1R3 and TRPV1/TRPV1t. Preference for 5% ethanol and 10% sucrose, CT responses to sweet stimuli, and T1R3 expression were greater in naive P rats than NP rats. The enhancement of the CT response to 0.5 M sucrose in the presence of varying ethanol concentrations (0.5-40%) in naive P rats was higher and shifted to lower ethanol concentrations than NP rats. Chronic ingestion of 5% sucrose or 5% ethanol decreased T1R3 mRNA in NP and P rats. Naive P rats also demonstrated bigger CT responses to NaCl+benzamil and greater TRPV1/TRPV1t expression. TRPV1t agonists produced biphasic effects on NaCl+benzamil CT responses, enhancing the response at low concentrations and inhibiting it at high concentrations. The concentration of a TRPV1/TRPV1t agonist (Maillard reacted peptides conjugated with galacturonic acid) that produced a maximum enhancement in the NaCl+benzamil CT response induced a decrease in NaCl intake and preference in P rats. In naive P rats and NP rats exposed to 5% ethanol in a no-choice paradigm, the biphasic TRPV1t agonist vs. NaCl+benzamil CT response profiles were higher and shifted to lower agonist concentrations than in naive NP rats. TRPV1/TRPV1t mRNA expression increased in NP rats but not in P rats exposed to 5% ethanol in a no-choice paradigm. We conclude that P and NP rats differ in T1R3 and TRPV1/TRPV1t expression and neural and behavioral responses to sweet and salty stimuli and to chronic sucrose and ethanol exposure.

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Section: Alcohol Preference and Sweet Tastementioning

confidence: 81%

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confidence: 99%

Strain differences in the neural, behavioral, and molecular correlates of sweet and salty taste in naive, ethanol- and sucrose-exposed P and NP rats

Coleman¹,

Williams²,

Phan³

et al. 2011

Journal of Neurophysiology

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“…In fact, their 0.2% saccharin preference declined from initial test (before saccharide tests) to test 3, and the KO mice strongly avoided 0.8% saccharin in test 3. Saccharin avoidance by KO mice has been attributed to the mice responding to the bitter taste component of the artificial sweetener (5). The saccharin avoidance by the KO mice in the last test clearly demonstrates that their sucrose preference in the second test does not represent a recovery of sweet taste sensitivity.…”

Section: Discussionmentioning

confidence: 99%

T1R3 taste receptor is critical for sucrose but not Polycose taste

Zukerman

Glendinning²,

Margolskee³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

117

167

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Zukerman S, Glendinning JI, Margolskee RF, Sclafani A. T1R3 taste receptor is critical for sucrose but not Polycose taste. In addition to their well-known preference for sugars, mice and rats avidly consume starch-derived glucose polymers (e.g., Polycose). T1R3 is a component of the mammalian sweet taste receptor that mediates the preference for sugars and artificial sweeteners in mammals. We examined the role of the T1R3 receptor in the ingestive response of mice to Polycose and sucrose. In 60-s two-bottle tests, knockout (KO) mice preferred Polycose solutions (4 -32%) to water, although their overall preference was lower than WT mice (82% vs. 94%). KO mice also preferred Polycose (0.5-32%) in 24-h two-bottle tests, although less so than WT mice at dilute concentrations (0.5-4%). In contrast, KO mice failed to prefer sucrose to water in 60-s tests. In 24-h tests, KO mice were indifferent to 0.5-8% sucrose, but preferred 16 -32% sucrose; this latter result may reflect the post-oral effects of sucrose. Overall sucrose preference and intake were substantially less in KO mice than WT mice. However, when retested with 0.5-32% sucrose solutions, the KO mice preferred all sucrose concentrations, although they drank less sugar than WT mice. The experience-induced sucrose preference is attributed to a post-oral conditioned preference for the T1R3-independent orosensory features of the sugar solutions (odor, texture, T1R2-mediated taste). Chorda tympani nerve recordings revealed virtually no response to sucrose in KO mice, but a near-normal response to Polycose. These results indicate that the T1R3 receptor plays a critical role in the tastemediated response to sucrose but not Polycose.preference; C57BL/6J mice; chorda tympani nerve; saccharin; postoral conditioning THE TASTE OF SUGAR IS HIGHLY attractive to humans and many other animal species. Studies of inbred mouse strains led to the identification of the T1R2 and T1R3 receptor proteins that dimerize to form a sweet taste receptor (1). Selective elimination of these receptor proteins in knockout mice attenuates or completely blocks the behavioral and gustatory nerve responses to sugars and artificial sweeteners (7, 40). Further, allelic variation in the Tas1r3 gene, which codes for the T1R3 protein (3,(17)(18)(19)24), contributes to strain differences in sensitivity (9), lick responsiveness (8, 10), peripheral taste nerve responsiveness (11), and daily intake and preference (11, 22) for sugars and artificial sweeteners.Sugars are not the only carbohydrates that have an attractive taste to some nonhuman species. Twenty years ago, our laboratory published a series of papers demonstrating that rats, mice, hamsters, and gerbils are strongly attracted to the taste of starch-derived glucose polymers such as Polycose and other maltodextrins (26). Behavioral and electrophysiological evidence indicates that Polycose and sucrose have qualitatively distinct taste sensations in rodents. For example, aversions conditioned to Polycose or sucrose do not cross-generalize, and some ta...

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“…Prior genetic mapping studies in mice have revealed a common chromosomal locus contributing to alcohol and sweetener consumption (the Ap3q alcohol preference/Sac locus; Bachmanov et al 2002) Nelson et al 2001;Sainz et al 2001;Zhao et al 2003). Knockout mice lacking the T1r3 receptor display substantially reduced intake of and preference for alcohol and sweet stimuli, but normal intake of other tastants, relative to B6 wild-type mice (Blednov et al 2008;Brasser et al 2010). Moreover, central taste-sensitive neurons in T1r3 receptordeficient mice show suppressed electrophysiological responses to oral ethanol and sweet stimuli, but not other tastants, relative to B6 control animals (Brasser et al 2010).…”

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confidence: 99%

Differential neural representation of oral ethanol by central taste-sensitive neurons in ethanol-preferring and genetically heterogeneous rats

Lemon

Wilson

Brasser

2011

Journal of Neurophysiology

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Lemon CH, Wilson DM, Brasser SM. Differential neural representation of oral ethanol by central taste-sensitive neurons in ethanol-preferring and genetically heterogeneous rats. J Neurophysiol 106: 3145-3156, 2011. First published September 14, 2011 doi:10.1152/jn.00580.2011In randomly bred rats, orally applied ethanol stimulates neural substrates for appetitive sweet taste. To study associations between ethanol's oral sensory characteristics and genetically mediated ethanol preference, we made electrophysiological recordings of oral responses (spike density) by taste-sensitive nucleus tractus solitarii neurons in anesthetized selectively bred ethanol-preferring (P) rats and their genetically heterogeneous Wistar (W) control strain. Stimuli (25 total) included ethanol [3%, 5%, 10%, 15%, 25%, and 40% (vol/vol)], a sucrose series (0.01, 0.03, 0.1, 0.3, 0.5, and 1 M), and other sweet, salt, acidic, and bitter stimuli; 50 P and 39 W neurons were sampled. k-means clustering applied to the sucrose response series identified cells showing high (S 1 ) or relatively low (S 0 ) sensitivity to sucrose. A three-way factorial analysis revealed that activity to ethanol was influenced by a neuron's sensitivity to sucrose, ethanol concentration, and rat line (P ϭ 0.01). Ethanol produced concentration-dependent responses in S 1 neurons that were larger than those in S 0 cells. Although responses to ethanol by S 1 cells did not differ between lines, neuronal firing rates to ethanol in S 0 cells increased across concentration only in P rats. Correlation and multivariate analyses revealed that ethanol evoked responses in W neurons that were strongly and selectively associated with activity to sweet stimuli, whereas responses to ethanol by P neurons were not easily associated with activity to representative sweet, sodium salt, acidic, or bitter stimuli. These findings show differential central neural representation of oral ethanol between genetically heterogeneous rats and P rats genetically selected to prefer alcohol.

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Perception of sweet taste is important for voluntary alcohol consumption in mice

Cited by 70 publications

References 76 publications

Strain differences in the neural, behavioral, and molecular correlates of sweet and salty taste in naive, ethanol- and sucrose-exposed P and NP rats

Strain differences in the neural, behavioral, and molecular correlates of sweet and salty taste in naive, ethanol- and sucrose-exposed P and NP rats

T1R3 taste receptor is critical for sucrose but not Polycose taste

Differential neural representation of oral ethanol by central taste-sensitive neurons in ethanol-preferring and genetically heterogeneous rats

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