Exendin-4 decreases amphetamine-induced locomotor activity

Erreger, Kevin; Davis, Adeola R.; Poe, Amanda; Greig, Nigel H.; Stanwood, Gregg D.; Galli, Aurelio

doi:10.1016/j.physbeh.2012.03.014

Cited by 79 publications

(65 citation statements)

References 66 publications

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“…Similar finding were reported in rats where the locomotor response precipitated by the psycho stimulant amphetamine was modulated by the administration of GLP-1 [7]. These findings have not yet been replicated in humans.…”

Section: Introductionsupporting

confidence: 78%

“…The LEAD-3 study attributed non-significant improvements in anxiety to globally increased satisfaction with improved glycaemic control and weight reduction, rather than to a central effect of the GLP-1 analogue per se [11]. Given the evidence from animal studies of GLP-1-induced reduction in alcohol intake and in the modulation of the locomotor response precipitated by amphetamine indicates that the reward centres (mesolimbic pathway) may have a role in this effect [6,7]. Further evidence of central action of exenatide in fMRI studies [13], supports this: although the exact mechanism whereby GLP-1 mediates an effect on anxiety remains unclear, it is likely to be associated with receptors in the mesolimbic system.…”

Section: Discussionmentioning

confidence: 99%

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Glucagon-Like Peptide-1 Analogues and Anxiety and Abnormal Eating Behaviours in Type 2 Diabetes: A Case Report

Doherty¹

2014

J Diabetes Metab

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Psychological and psychiatric problems are common in diabetes. Glucagon-like peptide-1 (GLP-1) analogues are effective in the management of type 2 diabetes as second or third-line treatment, and are thought to have a central effect on appetite regulation. There is little evidence regarding the effect of GLP-1 analogues on anxiety. This is a case report of a patient with type 2 diabetes, obesity, anxiety and disordered eating who was commenced on Liraglutide, a glucagon-like peptide-1 (GLP-1) analogue.This patient reported, in addition to improved glycaemic control, a marked improvement in the anxiety which had been present all her life, and had driven her binge eating. This anxiety had persisted despite anxiolytic medications and cognitive behaviour therapy.Any medication which could have a positive effect on anxiety and diabetes both would be valuable. Glucagon like peptide analogues may have a role in the management of co-morbid anxiety and type 2 diabetes. Further research is required into this area.

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Section: Introductionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Glucagon-Like Peptide-1 Analogues and Anxiety and Abnormal Eating Behaviours in Type 2 Diabetes: A Case Report

Doherty¹

2014

J Diabetes Metab

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“…Liraglutide was not detected outside of CVOs and hypothalamus, so the activation in these areas except AP may be indirect. There likely are important effects of GLP-1R in areas of the brain associated with reward, as GLP-1R agonists have been show to lead to changed food preference away from typically rewarding foods (79), and exendin-4 has been shown to reduce basal as well as amphetamine-induced locomotor activity, and reduced alcohol intake has also been reported (80,81).…”

Section: Surgery Models and Compound Administrationmentioning

confidence: 99%

The arcuate nucleus mediates GLP-1 receptor agonist liraglutide-dependent weight loss

Secher¹,

Jelsing²,

Baquero³

et al. 2014

J. Clin. Invest.

693

673

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“…Given that the limbic system is central for the rewarding properties of behavior, substances, and food (59), this is hardly surprising. In fact, several studies have concluded that activation of GLP-1R in the limbic system can attenuate the reward from the consumption of cocaine (19,27) or amphetamines (19,21), and even lead to reduced consumption of narcotics, such as alcohol (20,88). These observations also go hand in hand with the presence of GLP-1 receptor mRNA (65) and PPG projections to the VTA, bed nucleus of the stria terminalis (BNST), amygdala, NAc, and lateral septum (LS).…”

Section: Brain Glp-1 and Food Intakementioning

confidence: 99%

PPG neurons of the lower brain stem and their role in brain GLP-1 receptor activation

Trapp

Cork

2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Within the brain, glucagon-like peptide-1 (GLP-1) affects central autonomic neurons, including those controlling the cardiovascular system, thermogenesis, and energy balance. Additionally, GLP-1 influences the mesolimbic reward system to modulate the rewarding properties of palatable food. GLP-1 is produced in the gut and by hindbrain preproglucagon (PPG) neurons, located mainly in the nucleus tractus solitarii (NTS) and medullary intermediate reticular nucleus. Transgenic mice expressing glucagon promoter-driven yellow fluorescent protein revealed that PPG neurons not only project to central autonomic control regions and mesolimbic reward centers, but also strongly innervate spinal autonomic neurons. Therefore, these brain stem PPG neurons could directly modulate sympathetic outflow through their spinal inputs to sympathetic preganglionic neurons. Electrical recordings from PPG neurons in vitro have revealed that they receive synaptic inputs from vagal afferents entering via the solitary tract. Vagal afferents convey satiation to the brain from signals like postprandial gastric distention or activation of peripheral GLP-1 receptors. CCK and leptin, short-and long-term satiety peptides, respectively, increased the electrical activity of PPG neurons, while ghrelin, an orexigenic peptide, had no effect. These findings indicate that satiation is a main driver of PPG neuronal activation. They also show that PPG neurons are in a prime position to respond to both immediate and long-term indicators of energy and feeding status, enabling regulation of both energy balance and general autonomic homeostasis. This review discusses the question of whether PPG neurons, rather than gut-derived GLP-1, are providing the physiological substrate for the effects elicited by central nervous system GLP-1 receptor activation. appetite; brain stem; glucagon-like peptide-1; hippocampus; neuroanatomy FOR TWO DECADES, IT HAS BEEN known that glucagon-like peptide (GLP-1) reduces food intake by acting within the central nervous system (95). That first study showed through the use of the GLP-1 receptor antagonist exendin-9 (Ex9) that endogenous GLP-1 has the ability to suppress food intake and that this effect is dependent on the feeding state of the animal. While unequivocally showing that GLP-1 has a physiological role in brain, the source of centrally acting GLP-1 remains less clear. Does postprandially released GLP-1 from the enteroendocrine L-cells reach the central nervous system (CNS) from the circulation, despite its short half-life in the blood, or does the small number of preproglucagon (PPG) neurons in the lower brain stem (37,58,65) provide sufficient GLP-1 for the plethora of brain regions that express its receptor? Although this question remains largely unanswered, it is clear that central GLP-1 is integral to many more processes linked to energy homeostasis than simply food intake. This review provides a detailed account of the different actions of GLP-1 in the brain, with a particular emphasis on the potential role of the PPG...

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Exendin-4 decreases amphetamine-induced locomotor activity

Cited by 79 publications

References 66 publications

Glucagon-Like Peptide-1 Analogues and Anxiety and Abnormal Eating Behaviours in Type 2 Diabetes: A Case Report

Glucagon-Like Peptide-1 Analogues and Anxiety and Abnormal Eating Behaviours in Type 2 Diabetes: A Case Report

The arcuate nucleus mediates GLP-1 receptor agonist liraglutide-dependent weight loss

PPG neurons of the lower brain stem and their role in brain GLP-1 receptor activation

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