Experience with Sugar Modifies Behavioral but not Taste-Evoked Medullary Responses to Sweeteners in Mice

Abstract

Dietary exposure to sugars increases the preference for and intake of sugar solutions in mice. We used brief-access lick tests and multiunit electrophysiological recordings from the nucleus of the solitary tract (NST) to investigate the role of taste in diet-induced changes in sucrose responsiveness. We exposed C57BL/6J (B6) and 129X1/SvJ (129) mice to either a sucrose diet (chow, water, and a 500mM sucrose solution) or a control diet (chow and water) for 3 days. In B6 mice, exposure to the sucrose diet decreased the appetitive response (i.e., number of trials initiated) but had no effect on the consummatory response (i.e., rate of licking) to 500mM sucrose and 20mM saccharin. In 129 mice, exposure to the sucrose diet increased the appetitive response but had no effect on the consummatory response to the sweetener solutions. In the NST recordings, the B6 mice exhibited larger multiunit responses to sweeteners than 129 mice, but there was no effect of the sucrose diet in either strain. Our results indicate that sucrose exposure alters the appetitive response of B6 and 129 mice to sweeteners in diametrically opposed ways and that these changes are mediated by structures in the gustatory neuraxis above the NST (e.g., ventral forebrain).

Cocaine decreases saccharin preference without altering sweet taste sensitivity

“…In brief-access lickometry, taste stimuli are presented for a short (seconds) duration. The output lick rate is not directly related to consumption in calories or volume, but instead, is a function of orosensory detection with minimal influence from post-ingestive effects (Glendinning et al , 2002, Loney et al , 2012, McCaughey and Glendinning, 2013). …”

“…We used a brief-access lickometer assay, as it is commonly used to identify taste quality and to separate orosensory-mediated responses from higher order responses (Loney et al , 2012, Mantella and Youngentob, 2014, McCaughey and Glendinning, 2013). This assay has been used to quantify differences of taste sensitivity in mice with mutations in taste-related genes (Tordoff and Ellis, 2013, Treesukosol et al , 2009) and to compare orosensory ability and drug preference for both nicotine (Glatt et al , 2009) and alcohol (Brasser et al , 2012).…”

Taste Responsiveness to Sweeteners Is Resistant to Elevations in Plasma Leptin

“…Another measure of ingestive responsiveness is the number of trials that mice initiated across the 30-min test session (McCaughey and Glendinning 2013). However, there were no significant differences in number of trials initiated by sham-and leptin-injected mice when tested with the broad (sham: 41.2 ± 2.9; leptin: 34.7 ± 3.6; unpaired t value = 1.42, df = 12, P = 0.18) or narrow (sham: 38.4 ± 3.2, leptin: 36.3 ± 2.4; unpaired t value = 0.52, df = 26, P = 0.61) range of sucrose concentrations.…”

Confection Confusion: Interplay Between Diet, Taste, and Nutrition

“…Consistent with this, rats fed a high-fat and high-sugar diet (45% fat and 17% sugar) for 8 weeks presented dulled nucleus tractus solitarius (NTS; Boxes 1 and 2 ) responses to taste that included lower magnitude and duration and longer latency to sweet solutions and naturalistic taste stimuli [ 44 ]. However, these changes seem to require an extended exposure to dietary sugar because previous work reported an increase in CT responses to sucrose and no changes in the NTS responses following a short, 3-day access to a high-energy diet (45% fat and 17% sugar) [ 45 ] or to a 0.5 M sucrose solution [ 46 ], respectively. These findings are especially interesting when compared with those of two studies in which mice fed a high-fat diet (60% fat and 22% carbohydrates) for 8 weeks showed a decrease in the number of taste buds responsive to sweet stimuli (saccharin and Acesulfame K) and in the amplitude of their calcium responses measured ex vivo with calcium-sensitive dyes [ 47 , 100 ].…”