Presynaptically mediated effects of cholecystokinin-8 on the excitability of area postrema neurons in rat brain slices

Sugeta, Shingo; Hirai, Yoshito; Maezawa, Hitoshi; Inoue, Nozomu; Yamazaki, Yutaka; Funahashi, Makoto

doi:10.1016/j.brainres.2015.05.018

Cited by 11 publications

(8 citation statements)

References 37 publications

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“…For example, the use of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist cyanquixaline to block amylin-induced excitatory responses revealed that administration of amylin excites AP neurons by facilitating glutamate release from glutamatergic inputs to AP neurons. Similar effects have been identified for CCK [ 94 , 106 ]. Interestingly, heterogenous responsiveness of AP neurons to metabolic factors has also been demonstrated.…”

Section: Anatomy and Potential Metabolic Role Of The Sensory Cvossupporting

confidence: 80%

“…Additionally, receptors for Ang-II, AVP, estrogen, and potentially insulin have also been identified in the AP [ 84 , 85 , 86 , 87 , 88 ]. Further characterization of receptor expression in specific cell types has revealed that amylin, leptin, Ang-II, GLP-1, adiponectin 1/2, CCK, and ghrelin receptors are expressed in AP neurons [ 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 ]. Leptin, TLR-4, glial-cell derived neurotrophic factor receptor

-like (GFRAL) and complement type 3 (a receptor linked to hypoxia-induced emesis) receptors are also localized on glial cells in this brain region [ 97 , 98 , 99 , 100 ].…”

Section: Anatomy and Potential Metabolic Role Of The Sensory Cvosmentioning

confidence: 99%

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Sensory Circumventricular Organs, Neuroendocrine Control, and Metabolic Regulation

2021

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The central nervous system is critical in metabolic regulation, and accumulating evidence points to a distributed network of brain regions involved in energy homeostasis. This is accomplished, in part, by integrating peripheral and central metabolic information and subsequently modulating neuroendocrine outputs through the paraventricular and supraoptic nucleus of the hypothalamus. However, these hypothalamic nuclei are generally protected by a blood-brain-barrier limiting their ability to directly sense circulating metabolic signals—pointing to possible involvement of upstream brain nuclei. In this regard, sensory circumventricular organs (CVOs), brain sites traditionally recognized in thirst/fluid and cardiovascular regulation, are emerging as potential sites through which circulating metabolic substances influence neuroendocrine control. The sensory CVOs, including the subfornical organ, organum vasculosum of the lamina terminalis, and area postrema, are located outside the blood-brain-barrier, possess cellular machinery to sense the metabolic interior milieu, and establish complex neural networks to hypothalamic neuroendocrine nuclei. Here, evidence for a potential role of sensory CVO-hypothalamic neuroendocrine networks in energy homeostasis is presented.

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Section: Anatomy and Potential Metabolic Role Of The Sensory Cvossupporting

confidence: 80%

-like (GFRAL) and complement type 3 (a receptor linked to hypoxia-induced emesis) receptors are also localized on glial cells in this brain region [ 97 , 98 , 99 , 100 ].…”

Section: Anatomy and Potential Metabolic Role Of The Sensory Cvosmentioning

confidence: 99%

Sensory Circumventricular Organs, Neuroendocrine Control, and Metabolic Regulation

2021

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“…(B) The CCK-BR, which mediates the physiological responses evoked by NS CCK, is distributed in the gastrointestinal tract (Sayegh, 2013a;Reubi et al, 1997;Monstein et al, 1996;Mantyh et al, 1994) and central areas that control food intake e.g. paraventricular nucleus of the hypothalamus, locus coeruleus, area postrema (AP), nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus (DMV) (Sugeta et al, 2015;Monnikes et al, 1997;O'Shea & Gundlach, 1993). (C) The vagus nerve, which comprises the major parasympathetic extrinsic innervation of the gut and communicates the satiety signals between the gut and the central feeding areas mentioned previously, also expresses CCK-BR (Dockray et al, 1981;Moriarty et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Non-sulfated cholecystokinin-8 reduces meal size and prolongs the intermeal interval in male Sprague Dawley rats

et al. 2019

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The current study measured seven feeding responses by non-sulfated cholecystokinin-8 (NS CCK-8) in freely fed adult male Sprague Dawley rats. The peptide (0, 0.5, 1, 3, 5 and 10nmol/kg) was given intraperitoneally (ip) prior to the onset of the dark cycle, and first meal size (MS), second meal size, intermeal interval (IMI) length, satiety ratio (SR = IMI/MS), latency to first meal, duration of first meal, number of meals and 24-hour food intake were measured. We found that NS CCK-8 (0.5 and 1.0nmol/kg) reduced MS, prolonged IMI length and increased SR during the dark cycle. Furthermore, the specific CCK-B receptor antagonist L365, 260 (1 mg/kg, ip) attenuated these responses. These results support a possible role for NS CCK-8 in regulating food intake.

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“…One potential site is a peripheral/ local/gastrointestinal site. One line of evidence pointing at this possibility is that two non-sulfated forms of CCK, CCK-8 and CCK-4, does not cross the blood brain barrier (Hagino et al, 1989;Sugeta et al, 2015). Therefore, the actions of NS CCK-8, possibly including reduction of food intake, may be peripheral/local i.e., gastrointestinal.…”

Section: Discussionmentioning

confidence: 99%

Non-sulfated cholecystokinin-8 increases enteric and hindbrain Fos-like immunoreactivity in male Sprague Dawley rats

et al. 2019

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Recently, we reported that non-sulfated cholecystokinin-8 (NS CCK-8) reduces food intake by cholecystokinin-B receptors (CCK-BR). To examine a possible site of action for this peptide, and based on the fact that both NS CCK-8 and CCK-BR are found centrally and peripherally, in the current study we hypothesized that NS CCK-8 increases Fos-like immunoreactivity (Fos-LI, a neuronal activation marker) in the dorsal vagal complex (DVC) of the hindbrain and the myenteric and submucosal plexuses of the small intestine. We found that intraperitoneal NS CCK-8 (0.5 nmol/kg) increases Fos-LI in the DVC, the myenteric and the submucosal plexuses of the duodenum and the myenteric plexus of the jejunum. The findings suggest, but does not prove, a potential role for the DVC and the enteric neurons in the feeding responses evoked by NS CCK-8.

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Presynaptically mediated effects of cholecystokinin-8 on the excitability of area postrema neurons in rat brain slices

Cited by 11 publications

References 37 publications

Sensory Circumventricular Organs, Neuroendocrine Control, and Metabolic Regulation

Sensory Circumventricular Organs, Neuroendocrine Control, and Metabolic Regulation

Non-sulfated cholecystokinin-8 reduces meal size and prolongs the intermeal interval in male Sprague Dawley rats

Non-sulfated cholecystokinin-8 increases enteric and hindbrain Fos-like immunoreactivity in male Sprague Dawley rats

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