Starvation-induced hyperactivity in the rat: The role of endocrine and neurotransmitter changes

Pirke, Karl M.; Broocks, Andreas; Wilckens, Thomas; Marquard, R.; Schweiger, Ulrich

doi:10.1016/s0149-7634(05)80012-0

Cited by 113 publications

(78 citation statements)

References 30 publications

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“…Recently it was shown that 5-HT 2C receptors, which are located on pro-opiomelanocortin (POMC) neurons in the arcuate nucleus, mediate the appetite-suppressant effects of d-fenfluramine (Heisler et al 2002). In our study we have shown that olanzapine treatment decreases RWA; however, it was previously shown that fluoxetine (SSRI) and 5-HT 2A/2C agonists also decrease RWA (Altemus et al 1996;Pirke et al 1993). Regarding conflicting data on serotonergic control of RWA, the possible involvement of other neurotransmitters should not be ignored.…”

Section: Discussionmentioning

confidence: 51%

Olanzapine Reduces Physical Activity in Rats Exposed to Activity-Based Anorexia: Possible Implications for Treatment of Anorexia Nervosa?

Hillebrand

Elburg

Kas

et al. 2005

Biological Psychiatry

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Section: Discussionmentioning

confidence: 51%

Olanzapine Reduces Physical Activity in Rats Exposed to Activity-Based Anorexia: Possible Implications for Treatment of Anorexia Nervosa?

Hillebrand

Elburg

Kas

et al. 2005

Biological Psychiatry

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“…"Activity/stress" model animals develop starvation-induced immunodeficiency and atrophy of the spleen and thymus (Watanabe et al 1992), as well as stress ulcers (Paré 1975), complications not observed in individuals with AN. In this model, administration of L-tryptophan and serotonin agonists and antagonists reduced physical activity (Pirke et al 1993) and tyrosine supplementation improved appetite and cognitive function and delayed the onset of fatigue in mice . Just as activity levels and restlessness in AN are sustained by a negative energy balance and low plasma leptin concentrations (van Elburg et al 2007), hypoleptinemia (Hebebrand et al 1997) and low glucose levels increase wheel running in rats (Takeda et al 2003).…”

Section: Animal Models Of Anmentioning

confidence: 97%

Relevance of animal models to human eating disorders and obesity

2008

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Background and rationale This review addresses the role animal models play in contributing to our knowledge about the eating disorders anorexia nervosa (AN) and bulimia nervosa (BN) and obesity. Objectives Explore the usefulness of animal models in complex biobehavioral familial conditions, such as AN, BN, and obesity, that involve interactions among genetic, physiologic, psychological, and cultural factors. Results and conclusionsThe most promising animal model to mimic AN is the activity-based anorexia rodent model leading to pathological weight loss. The paradigm incorporates reward elements of the drive for activity in the presence of an appetite and allows the use of genetically modified animals. For BN, the sham-feeding preparation in rodents equipped with a gastric fistula appears to be best suited to reproduce the postprandial emesis and the defects in satiety. Animal models that incorporate genes linked to behavior and mood may clarify biobehavioral processes underlying AN and BN. By contrast, a relative abundance of animal models has contributed to our understanding of human obesity. Both environmental and genetic determinants of obesity have been modeled in rodents. Here, we consider single gene mutant obesity models, along with models of obesigenic environmental conditions. The contributions of animal models to obesity research are illustrated by their utility for identifying genes linked to human obesity, for elucidating the pathways that regulate body weight and for the identification of potential therapeutic targets. The utility of these models may be further improved by exploring the impact of experimental manipulations on the behavioral determinants of energy balance.

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“…Depending on the animal species examined, both decreases and increases in locomotor activity have been described in response to limited food supplies (Pirke et al, 1993;Weed et al, 1997;Geng et al, 2007;Teske and Kotz, 2009;Boehm et al, 2010;Gingerich et al, 2010;Yu et al, 2010). However, gait-specific effects have not been considered.…”

Section: Received 1 November 2013; Accepted 10 April 2014mentioning

confidence: 99%

“…In addition, starved shrimp (Yu et al, 2010) and fish (Gingerich et al, 2010) decrease their swimming speed. In contrast, rats show hyperactive wheel running in response to starvation (Koubi et al, 1991;Pirke et al, 1993). Similarly, caloric restriction increases physical activity in rats (Geng et al, 2007;Teske and Kotz, 2009) and rhesus monkeys (Weed et al, 1997).…”

Section: Research Articlementioning

confidence: 99%

Gait-specific adaptation of locomotor activity in response to dietary restriction inCaenorhabditis elegans

Lüersen

Faust

Gottschling

et al. 2014

Journal of Experimental Biology

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Locomotion is crucial for the survival of living organisms, as it allows foraging, flight and mating behaviour. In response to environmental cues, many organisms switch between alternative forms of locomotion, referred to as gaits. The nematode Caenorhabditis elegans exhibits two gaits: swimming in liquids and crawling on dense gels. The kinematics and patterns of muscle activity differ between the two gaits, with swimming being less efficient than crawling. We found that C. elegans when grown on dietary restriction (DR) plates and then tested immediately for swimming activity exhibit an accelerated frequency of body-bending swimming compared with ad libitum-fed worms, resulting in an increased swimming speed. This response is independent of the presence or absence of food bacteria in the assay liquid. In contrast, the crawling speed of DR worms on assay agar plates is decreased and influenced by food availability. Because DR also attenuates the disturbed swimming activity of worms that are deficient in the presynaptic dopamine transporter DAT-1, our data link DR-induced alterations of the swimming gait to synaptic processes. This strongly suggests a biochemical rather than a biomechanical response to DR provoked by changes in the worm's body structure. We conclude that the increase in locomotor activity in response to DR is specific to the swimming gait and might represent a survival strategy, allowing food-deprived nematodes to exit unfavourable environments.

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Starvation-induced hyperactivity in the rat: The role of endocrine and neurotransmitter changes

Cited by 113 publications

References 30 publications

Olanzapine Reduces Physical Activity in Rats Exposed to Activity-Based Anorexia: Possible Implications for Treatment of Anorexia Nervosa?

Olanzapine Reduces Physical Activity in Rats Exposed to Activity-Based Anorexia: Possible Implications for Treatment of Anorexia Nervosa?

Relevance of animal models to human eating disorders and obesity

Gait-specific adaptation of locomotor activity in response to dietary restriction inCaenorhabditis elegans

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