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Description
The unpleasant bitter taste found in many nutritious vegetables may deter their consumption. While bitterness suppression by prototypical tastants is well-studied in the chemical and pharmacological fields, mechanisms to reduce the bitterness of foods such as vegetables remain to be elucidated. Here tastants representing the taste primaries of

The unpleasant bitter taste found in many nutritious vegetables may deter their consumption. While bitterness suppression by prototypical tastants is well-studied in the chemical and pharmacological fields, mechanisms to reduce the bitterness of foods such as vegetables remain to be elucidated. Here tastants representing the taste primaries of salty and sweet were investigated as potential bitterness suppressors of three types of Brassicaceae vegetables. The secondary aim of these studies was to determine whether the bitter masking agents were differentially effective for bitter-sensitive and bitter-insensitive individuals. In all experiments, participants rated vegetables plain and with the addition of tastants. In Experiments 1-3, sucrose and NNS suppressed the bitterness of broccoli, Brussels sprouts, and cauliflower, whereas NaCl did not. Varying concentrations of NaCl and sucrose were introduced in Experiment 4 to assess the dose-dependency of the effects. While sucrose was a robust bitterness suppressor, NaCl suppressed bitterness only for participants who perceived the plain Brussels sprouts as highly bitter. Experiment 5, through the implementation of a rigorous control condition, determined that some but not all of this effect can be accounted for by regression to the mean. Individual variability in taste perception as determined by sampling of aqueous bitter, salty, and sweet solutions did not influence the degree of suppression by NaCl or sucrose. Consumption of vegetables is deterred by their bitter taste. Utilizing tastants to mask bitterness, a technique that preserves endogenous nutrients, can circumvent this issue. Sucrose is a robust bitter suppressor whereas the efficacy of NaCl is dependent upon bitterness perception of the plain vegetables.
ContributorsWilkie, Lynn Melissa (Author) / Capaldi Phillips, Elizabeth D (Thesis advisor) / Cohen, Adam (Committee member) / Johnston, Carol (Committee member) / Sanabria, Federico (Committee member) / Arizona State University (Publisher)
Created2014
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Description
Epidemiological studies have identified obesity as a risk factor for numerous chronic diseases such as adult onset diabetes, hypertension, and hypercholesterolemia. In both humans and laboratory animals, high-fat diets have been shown to cause obesity. Increases in dietary fat lead to increased energy consumption and, consequently, significant increases in body

Epidemiological studies have identified obesity as a risk factor for numerous chronic diseases such as adult onset diabetes, hypertension, and hypercholesterolemia. In both humans and laboratory animals, high-fat diets have been shown to cause obesity. Increases in dietary fat lead to increased energy consumption and, consequently, significant increases in body fat content. CD36 has been implicated in fat perception, preference, and increased consumption, but it is yet to be tested using a behavior paradigm. To study the effect of CD36 on fat taste transmission and fat consumption, four CD36 knockout (experimental) mice and four Black 6 wildtype (control) mice underwent 20 days of fat preference and perception testing. Both groups of mice were exposed to foods with progressively increasing fat content (10%, 12.5%, 15% 17.5%, 20%, 45%) in order to assess the effect of CD36 on fat preference. Afterward, the mice were subjected to an aversive conditioning protocol designed to test the effect of CD36 on fat taste perception; development of a conditioned taste aversion was indicative of ability to taste fat. Especially, knockout mice exhibited diminished preference for and reduced consumption of fat during preference testing and were unable to identify fat taste as the conditioned stimulus during aversive conditioning. A repeated measures ANOVA with Bonferroni correction revealed a significant main effect of group on fat consumption, energy intake, and weight. Linear regression revealed CD36 status to account for a majority of observed variance in fat consumption across both phases of the experiment. These results implicate CD36 in fat taste perception and preference and add to the growing body of evidence suggesting fat as a primary taste.
ContributorsJasbi, Paniz (Author) / Johnston, Carol (Thesis advisor) / Lespron, Christy (Committee member) / Wadhera, Devina (Committee member) / Arizona State University (Publisher)
Created2018
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Description
Timing performance is sensitive to fluctuations in time and motivation, thus interval timing and motivation are either inseparable or conflated processes. A behavioral systems model (e.g., Timberlake, 2000) of timing performance (Chapter 1) suggests that timing performance in externally-initiated (EI) procedures conflates behavioral modes differentially sensitive to motivation, but that

Timing performance is sensitive to fluctuations in time and motivation, thus interval timing and motivation are either inseparable or conflated processes. A behavioral systems model (e.g., Timberlake, 2000) of timing performance (Chapter 1) suggests that timing performance in externally-initiated (EI) procedures conflates behavioral modes differentially sensitive to motivation, but that response-initiated (RI) procedures potentially dissociate these behavioral modes. That is, timing performance in RI procedures is expected to not conflate these behavioral modes. According to the discriminative RI hypothesis, as initiating-responses become progressively discriminable from target responses, initiating-responses increasingly dissociate interval timing and motivation. Rats were trained in timing procedures in which a switch from a Short to a Long interval indexes timing performance (a latency-to-switch, LTS), and were then challenged with pre-feeding and extinction probes. In experiments 1 (Chapter 2) and 2 (Chapter 3), discriminability of initiating-responses was varied as a function of time, location, and form for rats trained in a switch-timing procedure. In experiment 3 (Chapter 4), the generalizability of the discriminative RI hypothesis was evaluated in rats trained in a temporal bisection procedure. In experiment 3, but not 1 and 2, RI enhanced temporal control of LTSs relative to EI. In experiments 1 and 2, the robustness of LTS medians to pre-feeding but not extinction increased with the discriminability of initiating-responses from target responses. In experiment 3, the mean LTS was robust to pre-feeding in EI and RI. In all three experiments, pre-feeding increased LTS variability in EI and RI. These results provide moderate support for the discriminative RI hypothesis, indicating that initiating-responses selectively and partially dissociate interval timing and motivation processes. Implications for the study of cognition and motivation processes are discussed (Chapter 5).
ContributorsDaniels, Carter W (Author) / Sanabria, Federico (Thesis advisor) / McClure, Samuel M. (Committee member) / Wynne, Clive D.L. (Committee member) / Olive, Michael F. (Committee member) / Arizona State University (Publisher)
Created2018
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Description
The capacity to track time in the seconds-to-minutes range, or interval timing, appears to be at least partially dependent on intact hippocampal (HPC) function. The current dissertation sought to dissociate timed responses, non-timed responses, and motivational aspects of behavior in order to propose a role of the HPC in specific

The capacity to track time in the seconds-to-minutes range, or interval timing, appears to be at least partially dependent on intact hippocampal (HPC) function. The current dissertation sought to dissociate timed responses, non-timed responses, and motivational aspects of behavior in order to propose a role of the HPC in specific timing sub-processes. In Chapter 2, effects of dorsal HPC (dHPC) lesions on temporal responding in a switch-timing task revealed a critical role of dHPC in the acquisition of interval timing criteria. Following dHPC lesions, the start time of responding was systemically shortened, in a manner that was enhanced and sustained when encoding a novel long interval, consistent with a memory-based account of dHPC function in timed responding. Chapter 3 investigated effects of chronic stress, which has been shown to reliably induce HPC dendritic retraction, on interval timing, utilizing response-initiated schedules of reinforcement, which facilitate deconvolution of timing and motivation. This revealed task-dependent effects on interval timing and motivation, where stress induced transient effects on motivation in a prospective timing task, but transient effects on the variability of timed responding in a retrospective timing task, consistent with an effect on memory function in interval timing. Chapter 4 sought to bring timed responding, motivation, and non-timed behaviors under stronger procedural control, through the implementation of a response-initiated timing-with-opportunity-cost task, in which a cost is imposed on temporal food-seeking by the presence of a concurrent source of probabilistic reinforcement. This arrangement garnered strong schedule control of behavior, and revealed individual-subject differences in the effects of reward devaluation, such that it affected motivation in some rats, but temporal responding in others. Using this methodology, Chapter 5 investigated initial temporal entrainment of behavior under pharmacological deactivation of dHPC and revealed its critical involvement in updating memory to new temporal contingencies. Together, data from this dissertation contrast with prior conclusions that the HPC is not involved in learning temporal criteria, and instead suggest that its function is indeed critical to encoding temporal intervals in memory.
ContributorsGupta, Tanya A. (Author) / Sanabria, Federico (Thesis advisor) / Conrad, Cheryl (Committee member) / Olive, Foster (Committee member) / McClure, Samuel (Committee member) / Arizona State University (Publisher)
Created2022