Terry L Davidson

American University Washington D.C., Washington, Washington, D.C., United States

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Publications (89)263.61 Total impact

  • Terry L. Davidson · Camille H. Sample · Scott E. Kanoski
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    ABSTRACT: Epidemiological studies indicate that Western diet intake, and the weight gain and obesity that it promotes, are associated not only with late-life dementia, but also with poorer cognitive flexibility and inhibitory control across the lifespan. In addition, rodents maintained on a Western diet are impaired on hippocampal-dependent inhibitory learning and memory tasks and exhibit increased blood-brain barrier permeability, hippocampal inflammation, and decreased hippocampal neurogenesis and plasticity. Interference with neuroendocrine signaling may also contribute to hippocampal dysfunction. As a consequence of these types of undesirable effects, Western diet intake may initiate a vicious cycle of progressive weight gain and cognitive decline. That is, consuming this diet induces hippocampal pathologies, which impair the ability to suppress retrieval of food-related memories. This impairment could promote further, and ultimately excessive, intake of the Western diet, leading to increasing weight gain and deteriorating cognitive functioning.
    No preview · Chapter · Dec 2015
  • Sara L Hargrave · Sabrina Jones · Terry L Davidson
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    ABSTRACT: Chronic failure to suppress intake during states of positive energy balance leads to weight gain and obesity. The ability to use context — including interoceptive satiety states — to inhibit responding to previously rewarded cues appears to depend on the functional integrity of the hippocampus. Recent evidence implicates energy dense Western diets in several types of hippocampal dysfunction, including reduced expression of neurotrophins and nutrient transporters, increased inflammation, microglial activation, and blood brain barrier permeability. The functional consequences of such insults include impairments in an animal's ability to modulate responding to previously reinforced cues. We propose that such deficits promote overeating, which can further exacerbate hippocampal dysfunction and thus initiate a vicious cycle of both obesity and progressive cognitive decline.
    No preview · Article · Dec 2015
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    Sara L. Hargrave · Terry L. Davidson · Wei Zheng · Kimberly P. Kinzig
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    ABSTRACT: Western diet (WD) intake induces obesity and metabolic dysfunction. The present study examined the effects of WD on hippocampal-dependent cognitive functioning and blood-brain barrier (BBB) permeability as a function of exposure duration, obesity phenotype, and peripheral markers of energy regulation. The use of hippocampal-dependent "place" or hippocampal-independent "response" strategies in a Y maze was assessed in male rats following 10, 40, and 90 days of WD exposure in diet-induced obese (DIO) rats, in diet resistant (DR) rats that are relatively insensitive to the obesogenic properties of WD, and in chow-fed controls. Insulin, glucose, and BBB permeability throughout several loci in the hippocampus, striatum, and cerebellum were evaluated in relation to duration of WD exposure, obesity phenotype, and type of strategy used. DIO rats had increased body weight and adiposity throughout the study, and elevated 10-day glucose and 90-day insulin levels. Throughout the study, chow-fed and DR rats reliably relied on a place strategy. DIO rats, in contrast, favored a response strategy at the 10- and 90-day time points. BBB leakage was observed in the dorsal striatum and multiple subregions of the hippocampus of DIO, but not DR or chow-fed rats. Increased ventral hippocampal BBB permeability and blood glucose levels were associated with reduced place strategy use. These data indicate that WD-induced BBB leakage is dependent on duration of diet exposure as well as obesity phenotype, and implicates BBB leakage and impaired glucoregulation in behavioral strategy and cognitive performance. (PsycINFO Database Record
    Full-text · Article · Nov 2015 · Behavioral Neuroscience
  • A.L. Riley · David Kearns · Sara Hargrave · Terry Davidson

    No preview · Article · Nov 2015
  • Terry L Davidson · Kerri N Boutelle

    No preview · Article · Jun 2015 · Appetite
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    ABSTRACT: In western and westernized societies, large portions of the population live in what are considered to be "obesogenic" environments. Among other things, obesogenic environments are characterized by a high prevalence of external cues that are associated with highly palatable, energy-dense foods. One prominent hypothesis suggests that these external cues become such powerful conditioned elicitors of appetitive and eating behavior that they overwhelm the internal, physiological mechanisms that serve to maintain energy balance. The present research investigated a learning mechanism that may underlie this loss of internal relative to external control. In Experiment 1, rats were provided with both auditory cues (external stimuli) and varying levels of food deprivation (internal stimuli) that they could use to solve a simple discrimination task. Despite having access to clearly discriminable external cues, we found that the deprivation cues gained substantial discriminative control over conditioned responding. Experiment 2 found that, compared to standard chow, maintenance on a "western-style" diet high in saturated fat and sugar weakened discriminative control by food deprivation cues, but did not impair learning when external cues were also trained as relevant discriminative signals for sucrose. Thus, eating a western-style diet contributed to a loss of internal control over appetitive behavior relative to external cues. We discuss how this relative loss of control by food deprivation signals may result from interference with hippocampal-dependent learning and memory processes, forming the basis of a vicious-cycle of excessive intake, body weight gain, and progressive cognitive decline that may begin very early in life. Copyright © 2015. Published by Elsevier Ltd.
    Full-text · Article · May 2015 · Appetite
  • Terry L. Davidson · Anthony L. Riley

    No preview · Article · May 2015 · American Scientist
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    Sara L Hargrave · Terry L Davidson · Tien-Jui Lee · Kimberly P Kinzig
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    ABSTRACT: Energy dense "Western" diets (WD) are known to cause obesity as well as learning and memory impairments, blood-brain barrier damage, and psychological disturbances. Impaired glucose (GLUT1) and monocarboxylate (MCT1) transport may play a role in diet-induced dementia development. In contrast, ketogenic diets (KD) have been shown to be neuroprotective. We assessed the effect of 10, 40 and 90 days WD, KD and Chow maintenance on spontaneous alternation (SA) and vicarious trial and error (VTE) behaviors in male rats, then analyzed blood glucose, insulin, and ketone levels; and hippocampal GLUT1 and MCT1 mRNA. Compared to Chow and KD, rats fed WD had increased 90 day insulin levels. SA was decreased in WD rats at 10, but not 40 or 90 days. VTE was perturbed in WD-fed rats, particularly at 10 and 90 days, indicating hippocampal deficits. WD rats had lower hippocampal GLUT1 and MCT1 expression compared to Chow and KD, and KD rats had increased 90 day MCT1 expression compared to Chow and WD. These data suggest that WD reduces glucose and monocarboxylate transport at the hippocampus, which may result in learning and memory deficits. Further, KD consumption may be useful for MCT1 transporter recovery, which may benefit cognition. Copyright © 2015. Published by Elsevier Ltd.
    Full-text · Article · Apr 2015 · Appetite
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    Terry L Davidson · Ashley A Martin
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    ABSTRACT: A recent study has found that obese women (but not men) have difficulty inhibiting food-rewarded, but not money-rewarded, appetitive behaviour, suggesting that obesity is associated with cognitive deficits that could selectively promote food intake, perhaps in a sex-dependent manner.
    Full-text · Article · Aug 2014 · Current Biology
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    ABSTRACT: This review describes how a cascade of associative relationships involving the sensory properties of foods, the nutritional consequences of their consumption and perceived internal states may play an important role in the learned control of energy intake and body weight regulation. In addition, we describe ways in which dietary factors in the current environment can promote excess energy intake and body weight gain by degrading these relationships or by interfering with the neural substrates that underlie the ability of animals to use them to predict the nutritive or energetic consequences of intake. We propose that an expanded appreciation of the diversity of orosensory, gastrointestinal, and energy state signals about which animals learn, combined with a greater understanding of predictive relationships in which these cues are embedded, will help generate new information and novel approaches to addressing the current global problems of obesity and metabolic disease.
    No preview · Article · Jul 2014 · Journal of Experimental Psychology: Animal Learning and Cognition
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    Terry L Davidson

    Preview · Article · Mar 2014 · American Journal of Clinical Nutrition
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    Ashley A Martin · Terry L Davidson
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    ABSTRACT: Evidence is accumulating which suggests that, in addition to leading to unprecedented rates of obesity, the current food environment is contributing to the development of cognitive impairment and dementia. Recent experimental research indicates that many of the cognitive deficits associated with obesity involve fundamental inhibitory processes that have important roles in the control of food intake, implicating these cognitive impairments as a risk factor for weight gain. Here, we review experiments that link obesity with deficits in memory, attentional, and behavioral control and contemplate how these deficits may predispose individuals to overeat. Specifically, we discuss how deficits in inhibitory control may reduce one's ability to resist eating when confronted with the variety of foods and food cues that are ubiquitous in today's environment. Special attention is given to the importance of memory inhibition to the control of eating and appetitive behavior, and the role of the hippocampus in this process. We also discuss the potential etiology of both obesity and obesity-related cognitive impairment, highlighting non-human animal research which links both of these effects to the consumption of the modern "Western" diet that is high in saturated fats and simple carbohydrates. We conclude that part of what makes the current food environment "obesogenic" is the increased presence of food cues and the increased consumption of a diet which compromises our ability to resist those cues. A multi-dimensional intervention which focuses on improving control over food-related cognitive processing may be useful not only for combating the obesity epidemic but also for minimizing the risk of serious cognitive disorder later in life.
    Full-text · Article · Mar 2014 · Physiology & Behavior
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    ABSTRACT: Intake of a Western diet (WD), which is high in saturated fat and sugar, is associated with deficits in hippocampal-dependent learning and memory processes as well as with markers of hippocampal pathology. In the present study, rats were trained to asymptote on hippocampal-dependent serial feature negative (FN) and hippocampal-independent simple discrimination problems. Performance was then assessed following 7 days on ad libitum chow and after 10, 24, 40, 60, and 90 days of maintenance on WD, on ketogenic (KETO) diet which is high in saturated fat and low in sugar and other carbohydrates, or continued maintenance on chow (CHOW). Confirming and extending previous findings, diet-induced obese (DIO) rats fed WD showed impaired FN performance, increased BBB permeability, and increased fasting blood glucose levels compared to CHOW controls and to diet resistant (DR) rats that did not become obese when maintained on WD. For rats fed the KETO diet, FN performance and BBB integrity was more closely associated with level of circulating ketone bodies than with obesity phenotype (DR or DIO) with higher levels of ketones appearing to provide a protective effect. The evidence also indicated that FN deficits preceded and predicted increased body weight and adiposity. This research (a) further substantiates previous findings of WD-induced deficits in hippocampal-dependent feature negative discriminations, (b) suggests that ketones may be protective against diet-induced cognitive impairment, and (c) provides evidence that diet-induced cognitive impairment precedes weight gain and obesity.
    Full-text · Article · Aug 2013 · Neuroscience
  • T.L. Davidson · C.H. Sample · S.E. Swithers
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    ABSTRACT: An enormous amount of research has been aimed at identifying biological and environmental factors that are contributing to the current global obesity pandemic. The present paper reviews recent findings which suggest that obesity is attributable, at least in part, to a disruption of the Pavlovian control of energy regulation. Within our framework, this disruption occurs when (a) consumption of sweet-tasting, but low calorie or noncaloric, foods and beverages reduces the ability of sweet tastes to predict the postingestive caloric consequences of intake and (b) consuming diets high in saturated fat and sugar (a.k.a., Western diet) impairs hippocampal-dependent learning and memory processes that are involved with the use of interoceptive "satiety" signals to anticipate when food and eating are not followed by appetitive postingestive outcomes. The paper concludes with discussion of a "vicious-cycle' model which links obesity to cognitive decline.
    No preview · Article · Jul 2013 · Neurobiology of Learning and Memory
  • Susan E Swithers · Camille H Sample · Terry L Davidson
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    ABSTRACT: The use of high-intensity sweeteners has been proposed as a method to combat increasing rates of overweight and obesity in the human population. However, previous work with male rats suggests that consumption of such sweeteners might contribute to, rather than ameliorate, weight gain. The goals of the present experiments were to assess whether intake of high-intensity sweeteners is associated with increased food intake and body weight gain in female rats; to evaluate whether this effect depends on composition of the maintenance diet (i.e., standard chow compared with diets high in energy, fat, and sugar [HE diets]); and to determine whether the phenotype of the rats with regard to propensity to gain weight on HE diets affects the consequences of consuming high-intensity sweeteners. The data demonstrated that female rats fed a low-fat, standard laboratory chow diet did not gain extra weight when fed yogurt dietary supplements sweetened with saccharin compared with those fed glucose-sweetened dietary supplements. However, female rats maintained on a "Westernized" diet high in fat and sugar (HE diet) showed significant increases in energy intake, weight gain, and adiposity when given saccharin-sweetened compared with glucose-sweetened yogurt supplements. These differences were most pronounced in female rats known to be prone to obesity prior to the introduction of the yogurt diets. Both selectively bred Crl:OP[CD] rats and outbred Sprague-Dawley rats fed an HE diet showing high levels of weight gain (diet-induced obese [DIO] rats) had increased weight gain in response to consuming saccharin-sweetened compared with glucose-sweetened supplements. However, in male rats fed an HE diet, saccharin-sweetened supplements produced extra weight gain regardless of obesity phenotype. These results suggest that the most negative consequences of consuming high-intensity sweeteners may occur in those most likely to use them for weight control, females consuming a "Westernized" diet and already prone to excess weight gain. (PsycINFO Database Record (c) 2013 APA, all rights reserved).
    No preview · Article · Feb 2013 · Behavioral Neuroscience
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    ABSTRACT: Background: An emerging literature suggests that environmental chemicals may play a role in the development of childhood obesity and metabolic disorders, especially when exposure occurs early in life. Objective: Here we assess the association between these health outcomes and exposure to maternal smoking during pregnancy as part of a broader effort to develop a research agenda to better understand the role of environmental chemicals as potential risk factors for obesity and metabolic disorders. Methods: PubMed was searched up to 8 March 2012 for epidemiological and experimental animal studies related to maternal smoking or nicotine exposure during pregnancy and childhood obesity or metabolic disorders at any age. A total of 101 studies—83 in humans and 18 in animals—were identified as the primary literature. Discussion: Current epidemiological data support a positive association between maternal smoking and increased risk of obesity or overweight in offspring. The data strongly suggest a causal relation, although the possibility that the association is attributable to unmeasured residual confounding cannot be completely ruled out. This conclusion is supported by findings from laboratory animals exposed to nicotine during development. The existing literature on human exposures does not support an association between maternal smoking during pregnancy and type 1 diabetes in offspring. Too few human studies have assessed outcomes related to type 2 diabetes or metabolic syndrome to reach conclusions based on patterns of findings. There may be a number of mechanistic pathways important for the development of aberrant metabolic outcomes following perinatal exposure to cigarette smoke, which remain largely unexplored. Conclusions: From a toxicological perspective, the linkages between maternal smoking during pregnancy and childhood overweight/obesity provide proof-of-concept of how early-life exposure to an environmental toxicant can be a risk factor for childhood obesity.
    Full-text · Article · Dec 2012 · Environmental Health Perspectives
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    ABSTRACT: In adult rats, data suggest that consumption of sweet tastes that do not deliver anticipated caloric consequences using high-intensity, non-caloric sweeteners, such as saccharin, interferes with learned relations that may contribute to energy balance. The goal of the present study was to assess the development of learning about sweet taste and calories by assessing whether pre-exposure to saccharin solutions reduces cue competition in pre-weanling rats. The results demonstrated that rats pre-exposed to saccharin and then trained with a novel grape flavor paired with a glucose-sweetened solution consumed more of the novel grape flavor presented alone than rats that had been pre-exposed to saccharin and given the grape flavor paired with water alone. No differences in intake of the novel grape flavor were observed in groups given pre-exposure to water or glucose solutions. Thus, by 15 days of age, rats appear to have established an association between sweet tastes and calories, and this association can be weakened by exposure to saccharin. © 2012 Wiley Periodicals, Inc. Dev Psychobiol.
    No preview · Article · Dec 2012 · Developmental Psychobiology
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    ABSTRACT: Rats that consume high-energy (HE) diets (i.e., diets high in saturated fats and sugar) show impaired hippocampal-dependent learning and memory (e.g., Kanoski and Davidson (2011) [1]). To further investigate this effect, we trained rats given restricted access to low-fat lab chow on hippocampal-dependent serial feature-negative (FN) and hippocampal-independent simple discrimination problems. When training was completed, Group Chow received ad libitum lab chow. The remaining rats received ad libitum HE diet. Performance on both discrimination problems was tested following 7, 14, 21 and 28 days of HE diet exposure. FN, but not simple discrimination, was abolished initially for all rats, and then re-emerged for Group Chow. For rats fed HE diet, those that weighed the least and had the lowest amount of body fat (HE-diet resistant (HE-DR) rats), performed like Group Chow on both discrimination problems. However, HE diet-induced obese (HE-DIO) rats (i.e., rats that weighed the most weight and had the most body fat) performed like Group Chow on the simple discrimination problem, but were impaired throughout testing on the FN problem. Subsequent assessment of blood-brain barrier (BBB) permeability revealed that concentrations of an exogenously administered dye were elevated in the hippocampus, but not in the striatum or prefrontal cortex for HE-DIO rats relative to the HE-DR and Chow groups. The results indicate that the adverse consequences of HE diet on hippocampal-dependent cognitive functioning are associated with detrimental effects on the BBB and that both of these outcomes vary with sensitivity to HE diet-induced increases in weight and adiposity.
    Full-text · Article · May 2012 · Physiology & Behavior
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    ABSTRACT: Previous work from our lab has demonstrated that experience with high-intensity sweeteners in rats leads to increased food intake, body weight gain and adiposity, along with diminished caloric compensation and decreased thermic effect of food. These changes may occur as a result of interfering with learned relations between the sweet taste of food and the caloric or nutritive consequences of consuming those foods. The present experiments determined whether experience with the high-intensity sweetener saccharin versus the caloric sweetener glucose affected blood glucose homeostasis. The results demonstrated that during oral glucose tolerance tests, blood glucose levels were more elevated in animals that had previously consumed the saccharin-sweetened supplements. In contrast, during glucose tolerance tests when a glucose solution was delivered directly into the stomach, no differences in blood glucose levels between the groups were observed. Differences in oral glucose tolerance responses were not accompanied by differences in insulin release; insulin release was similar in animals previously exposed to saccharin and those previously exposed to glucose. However, release of GLP-1 in response to an oral glucose tolerance test, but not to glucose tolerance tests delivered by gavage, was significantly lower in saccharin-exposed animals compared to glucose-exposed animals. Differences in both blood glucose and GLP-1 release in saccharin animals were rapid and transient, and suggest that one mechanism by which exposure to high-intensity sweeteners that interfere with a predictive relation between sweet tastes and calories may impair energy balance is by suppressing GLP-1 release, which could alter glucose homeostasis and reduce satiety.
    No preview · Article · Apr 2012 · Behavioural brain research
  • Leonard E Jarrard · Lisa P Luu · Terry L Davidson
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    ABSTRACT: This study examined structural-functional differences along the septo-temporal axis of hippocampus using radial-maze tasks that involved two different memory processes [reference memory (RM) and working memory (WM)], and the use of two kinds of information (spatial vs. nonspatial cue learning). In addition, retention of the nonspatial cue task was tested nine weeks following completion of acquisition, and the rats then underwent discrimination reversal training. Ibotenic acid lesions limited to either the dorsal pole, intermediate area, or ventral pole had minimal effects on acquisition of the complex place and cue discrimination tasks. The one exception was that rats with lesions confined to the dorsal third of hippocampus made more WM errors on the spatial task (but not the cue task) early in training. Selective lesions of the three hippocampal regions had no effects on either long-term retention or reversal of the nonspatial cue discrimination task. In contrast, rats that had all of the hippocampus removed were severely impaired in learning the spatial task, making many RM and WM errors, whereas on the nonspatial cue task, the impairment was limited to WM errors. Further analysis of the WM errors made in acquisition showed that rats with complete lesions were significantly more likely on both the spatial and nonspatial cue tasks to reenter arms that had been baited and visited on that trial compared to arms that had not been baited. A similar pattern of errors emerged for complete hippocampal lesioned rats during reversal discrimination. This pattern of errors suggests that in addition to an impairment in handling spatial information, complete removal of hippocampus also interferes with the ability to inhibit responding to cues that signal reward under some conditions but not under others. The finding that selective lesions limited to the intermediate zone of the hippocampus produce no impairment in either WM ("rapid place learning") or RM in our radial maze tasks serve to limit the generality of the conclusion of Bast et al. (Bast et al. (2009) PLos Biol 7:730-746) that the intermediate area is needed for behavioral performance based on rapid learning about spatial cues.
    No preview · Article · Apr 2012 · Hippocampus

Publication Stats

2k Citations
263.61 Total Impact Points


  • 2013-2015
    • American University Washington D.C.
      • Department of Psychology
      Washington, Washington, D.C., United States
  • 2014
    • University of Bristol
      • School of Experimental Psychology
      Bristol, England, United Kingdom
  • 1992-2013
    • Purdue University
      • • Department of Psychological Sciences
      • • Ingestive Behavior Research Center (IBRC)
      ウェストラファイエット, Indiana, United States
  • 2010
    • University of Pennsylvania
      • Department of Psychology
      Philadelphia, PA, United States
  • 2008
    • McGill University
      • School of Dietetics and Human Nutrition
      Montréal, Quebec, Canada
  • 2000
    • University of Cincinnati
      • Department of Psychiatry
      Cincinnati, Ohio, United States
  • 1993
    • Lee University
      Кливленд, Tennessee, United States
  • 1989-1991
    • Virginia Military Institute
      Lexington, Virginia, United States