Localization of orexin-1 receptors to vagal afferent neurons in the rat and humans

Burdyga, Galina; Lal, Simon; Spiller, David G.; Jiang, Weiwei; Thompson, David G.; Attwood, S. E. A.; Saeed, Shakeel R; Grundy, David; Varró, Andrea; Dimaline, R.; Dockray, Graham J.

doi:10.1053/gast.2003.50020

Cited by 98 publications

(86 citation statements)

References 32 publications

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“…Studies were made using adult male Wistar rats (250 -450 gm; Biomedical Services Unit, University of Liverpool) that were housed at 22°C under a 12 hr light/dark cycle with ad libitum access to food and water (unless stated otherwise). Samples of human vagal nerve trunks were obtained during resections for gastro-esophageal carcinoma and cleanly dissected from the serosa; in addition, nodose ganglia were obtained at resections for head and neck tumors (Burdyga et al, 2003). Human tissues were separated rapidly and either immersed in RNA later (Ambion, Austin, TX) or fixed in 4% paraformaldehyde for morphological studies.…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA was extracted from pooled (8 -14) rat nodose ganglia and from three human vagal trunks in Trizol Reagent (Invitrogen, Paisley, UK). Samples were treated with DNase, reverse transcribed, and processed for PCR using BIO-X-ACT DNA Polymerase (Bioline) using the primers listed in Table 1 as described previously (Burdyga et al, 2002(Burdyga et al, , 2003. PCR products were cloned directly into the pGEM-T Easy cloning vector (Promega, Madison, WI), and sequence analysis was performed using an automated dideoxy method.…”

Section: Methodsmentioning

confidence: 99%

“…Recent work suggests that several other neurohumoral factors may modulate the effects of CCK on vagal afferent nerve discharge. Thus receptors (Ob-R) for the long (functional) form of the satiety hormone leptin are expressed by the same vagal neurons that express CCK-1 receptors (Buyse et al, 2001;Burdyga et al, 2002;Peiser et al, 2002), and there are synergistic interactions between CCK and leptin for both inhibition of food intake (Barrachina et al, 1997) and afferent nerve discharge Conversely, the same population of neurons also expresses receptors for the orexigenic peptide orexin-A (OX-R1), which inhibits the stimulatory effect of CCK on vagal afferent nerve discharge (Burdyga et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Expression of Cannabinoid CB1 Receptors by Vagal Afferent Neurons Is Inhibited by Cholecystokinin

Burdyga¹,

Lal²,

Varró³

et al. 2004

J. Neurosci.

251

224

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Both inhibitory (satiety) and stimulatory (orexigenic) factors from the gastrointestinal tract regulate food intake. In the case of the satiety hormone cholecystokinin (CCK), these effects are mediated via vagal afferent neurons. We now report that vagal afferent neurons expressing the CCK-1 receptor also express cannabinoid CB1 receptors. Retrograde tracing established that these neurons project to the stomach and duodenum. The expression of CB1 receptors determined by RT-PCR, immunohistochemistry and in situ hybridization in rat nodose ganglia was increased by withdrawal of food for Ն12 hr. After refeeding of fasted rats there was a rapid loss of CB1 receptor expression identified by immunohistochemistry and in situ hybridization. These effects were blocked by administration of the CCK-1 receptor antagonist lorglumide and mimicked by administration of CCK to fasted rats. Because CCK is a satiety factor that acts via the vagus nerve and CB1 agonists stimulate food intake, the data suggest a new mechanism modulating the effect on food intake of satiety signals from the gastrointestinal tract.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Expression of Cannabinoid CB1 Receptors by Vagal Afferent Neurons Is Inhibited by Cholecystokinin

Burdyga¹,

Lal²,

Varró³

et al. 2004

J. Neurosci.

251

224

View full text Add to dashboard Cite

show abstract

“…A recent report [23] showed that orexin-1 receptors are present in neurons and SGCs in human and rat nodose ganglia, and in humans also SGCs displayed orexin-1 receptors. In view of the rising interest into the mechanisms of obesity it will be worth pursuing the role of SGCs in the signaling in this pathway.…”

Section: Receptors For Other Peptidesmentioning

confidence: 97%

Satellite glial cells in sensory ganglia: from form to function

Hanani

2005

Brain Research Reviews

648

744

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“…Th e DVC consists of the dorsal motor nucleus of the vagus (DVN), the area postrema (AP), and the NTS within which POMC neurons exist (Schwartz 2010). Receptors for a variety of hormones controlling food intake have been found to be expressed in the brainstem vagal aff erent neurons including cholecystokinin (CCK) 1R and CCK 2R at which both CCK and gastrin act (Moriarty et al 1997), insulin receptors, GLP-1 (Nakagawa et al 2004) and GLP-2R (Nelson et al 2007), growth hormone secretagogue receptor (GHS)-R1 at which ghrelin acts (Date et al 2002), the orexin receptor, OX-R1 (Burdyga et al 2003), and leptin (Burdyga et al 2002).…”

Section: Role Of the Brainstemmentioning

confidence: 99%

Central and peripheral control of food intake

Abdalla

2017

Endocrine Regulations

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Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. Th e obesity has an evil eff ect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity. Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive (Jequier and Tappy 1999). As a compensatory mechanism, hunger increases and energy expenditure decreases the weight loss. However, opposite responses are triggered when body weight increases. Body weight can change only when energy intake is not equal to energy expenditure over a given period of time (Bray et al. 2012). A complex physiological control system is involved in the maintenance of the energy balance. Th is system includes aff erent signals from the periphery about the state of the energy stores and eff erent signals that affect the energy intake and expenditure (Sandoval et al. 2008). Th is regulatory system is formed by multiple interactions between the gastrointestinal tract (GIT), adipose tissue, and the central nervous system (CNS). It is infl uenced by behavioral, sensorial, autonomic, nutritional, and endocrine mechanisms (Boguszewski et al. 2010). Satiety and adiposity signalsTh e food intake control includes a short-term regulation, which determines the beginning and the end of a meal (hunger and satiation) and the interval between the meals (satiety) and a long-term regulation with factors (signals of adiposity), which help to regulate the body energy depots (Cummings and Overduin 2007).Th e satiation means a suppression of the hunger and termination of the food intake aft er ingestion of Unauthenticated Download Date | 5/11/18 9:54 AM

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Localization of orexin-1 receptors to vagal afferent neurons in the rat and humans

Cited by 98 publications

References 32 publications

Expression of Cannabinoid CB1 Receptors by Vagal Afferent Neurons Is Inhibited by Cholecystokinin

Expression of Cannabinoid CB1 Receptors by Vagal Afferent Neurons Is Inhibited by Cholecystokinin

Satellite glial cells in sensory ganglia: from form to function

Central and peripheral control of food intake

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