Endogenous orexin-A in the brain mediates 2-deoxy-d-glucose-induced stimulation of gastric motility in freely moving conscious rats

Nozu, Tsukasa; Tuchiya, Yoshihiro; Kumei, Shima; Takakusaki, Kaoru; Ataka, Koji; Fujimiya, Mineko; Okumura, Toshikatsu

doi:10.1007/s00535-011-0506-7

Cited by 20 publications

(10 citation statements)

References 46 publications

(46 reference statements)

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“…In contrast, 2-DG-stimulated acid production was inhibited by nesfatin-1 in a dose-dependent manner. As 2-DG is known to trigger gastric acid secretion by activation of the vagal center (10,19,32), our study indicates that nesfatin-1 suppresses vagally stimulated gastric acid production.…”

Section: Discussionsupporting

confidence: 52%

“…Systemic administration of 2-DG initiates a state of simulated cytoglycopenia, leading to altered hypothalamic input to the dorsal-vagal complex (DVC) in the brain stem and resultant activation of bilateral vagus nerves (10,19,30). 2-DG has been widely used to study gastric acid secretion mediated by the vagus nerve (19,32,36). Using gastrin and 2-DG to evaluate peripheral and central mechanisms of stimulated acid production, we have explored the effects of centrally administered nesfatin-1 on gastric acid secretion.…”

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confidence: 99%

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Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats

Xia

Fritze

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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MW. Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats. Am J Physiol Gastrointest Liver Physiol 303: G570 -G577, 2012. First published June 21, 2012; doi:10.1152/ajpgi.00178.2012.-Nesfatin-1, a novel hypothalamic peptide, inhibits nocturnal feeding behavior and gastrointestinal motility in rodents. The effects of nesfatin-1 on gastrointestinal secretory function, including gastric acid production, have not been evaluated. Nesfatin-1 was injected into the fourth intracerebral ventricle (4V) of chronically cannulated rats to identify a nesfatin dose sufficient to inhibit food intake. Nesfatin-1 (2 g) inhibited dark-phase food intake, in a dose-dependent fashion, for Ͼ3 h. Gastric acid production was evaluated in urethane-anesthetized rats. Nesfatin-1 (2 g) was introduced via the 4V following endocrine stimulation of gastric acid secretion by pentagastrin (2 g·kg Ϫ1 ·h Ϫ1 iv), vagal stimulation with 2-deoxy-D-glucose (200 mg/kg sc), or no stimulus. Gastric secretions were collected via gastric cannula and neutralized by titration to determine acid content. Nesfatin-1 did not affect basal and pentagastrin-stimulated gastric acid secretion, whereas 2-deoxy-D-glucosestimulated gastric acid production was inhibited by nesfatin-1 in a dose-dependent manner. c-Fos immunofluorescence in brain sections was used to evaluate in vivo neuronal activation by nesfatin-1 administered via the 4V. Nesfatin-1 caused activation of efferent vagal neurons, as evidenced by a 16-fold increase in the mean number of c-Fos-positive neurons in the dorsal motor nucleus of the vagus (DMNV) in nesfatin-1-treated animals vs. controls (P Ͻ 0.01). Finally, nesfatin-induced Ca 2ϩ signaling was evaluated in primary cultured DMNV neurons from neonatal rats. Nesfatin-1 caused dosedependent Ca 2ϩ increments in 95% of cultured DMNV neurons. These studies demonstrate that central administration of nesfatin-1, at doses sufficient to inhibit food intake, results in inhibition of vagally stimulated secretion of gastric acid. Nesfatin-1 activates DMNV efferent vagal neurons in vivo and triggers Ca 2ϩ signaling in cultured DMNV neurons. gastric hormones; intracellular calcium; dorsal motor nucleus of the vagus NESFATIN-1, an 82-amino acid peptide derived from the parent peptide nucleobindin-2, was first identified as a satiety molecule in the hypothalamus by Oh et al. (33). Inhibition of rodent nocturnal feeding behavior by nesfatin-1 administered into the intracranial ventricles has been consistently observed (18,25,34,40,42). Most centrally acting peptides that influence food intake also regulate the processes of digestion, including gastrointestinal motility and secretory function (45). In rodents, nesfatin-1 inhibits gastroduodenal motility and gastric empty-

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Section: Discussionsupporting

confidence: 52%

mentioning

confidence: 99%

Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats

Xia

Fritze

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Consistent with our finding, previous studies have revealed that endogenous orexin systems play important roles in the regulation of gastrointestinal function, motor learning and visceral sensation. For example intracisternal injection of SB-334687 suppressed gastric contractions induced by central vagal stimulation or acute restraint stress (B€ ulb€ ul et al, 2010;Nozu et al, 2012). Furthermore, endogenous orexins modulated the activity of Purkinje cells in the cerebellum and therefore participated in motor learning (Chen et al, 2013).…”

Section: Endogenous Orexin-a Modulates the Spontaneous Firing Activitmentioning

confidence: 99%

Orexin‐A increases the activity of globus pallidus neurons in both normal and parkinsonian rats

Xue

Yang

Liu

et al. 2016

Eur J of Neuroscience

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Orexin is a member of neuropeptides which was first identified in the hypothalamus. The globus pallidus is a key structure in the basal ganglia, which is involved in both normal motor function and movement disorders. Morphological studies have shown the expression of both OX1 and OX2 receptors in the globus pallidus. Employing single unit extracellular recordings and behavioural tests, the direct in vivo electrophysiological and behavioural effects of orexin-A in the globus pallidus were studied. Micro-pressure administration of orexin-A significantly increased the spontaneous firing rate of pallidal neurons. Correlation analysis revealed a negative correlation between orexin-A induced excitation and the basal firing rate. Furthermore, application of the specific OX1 receptor antagonist, SB-334867, decreased the firing rate of pallidal neurons, suggesting that endogenous orexinergic systems modulate the firing activity of pallidal neurons. Orexin-A increased the excitability of pallidal neurons through both OX1 and OX2 receptors. In 6-hydroxydopamine parkinsonian rats, orexin-A-induced increase in firing rate of pallidal neurons was stronger than that in normal rats. Immunostaining revealed positive OX1 receptor expression in the globus pallidus of both normal and parkinsonian rats. Finally, postural test showed that unilateral microinjection of orexin-A led to contralateral deflection in the presence of systemic haloperidol administration. Further elevated body swing test revealed that pallidal orexin-A and SB-334867 induced contralateral-biased swing and ipsilateral-biased swing respectively. Based on the electrophysiological and behavioural findings of orexin-A in the globus pallidus, the present findings may provide a rationale for the pathogenesis and treatment of Parkinson's disease.

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“…The method used in the present study had already established well to measure GI contractions [13,[15][16][17][18]. Non-fasted rats were placed in a wire-bottom and non-restraint polycarbonate cage.…”

Section: Manometric Recordings and Study Designmentioning

confidence: 99%

Water-avoidance stress enhances gastric contractions in freely moving conscious rats: role of peripheral CRF receptors

et al. 2013

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Endogenous orexin-A in the brain mediates 2-deoxy-d-glucose-induced stimulation of gastric motility in freely moving conscious rats

Abstract: Running head; Orexin and gastric motility 2 Abstract Background. Increasing evidence has indicated that brain orexin plays a

Cited by 20 publications

References 46 publications

Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats

Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats

Orexin‐A increases the activity of globus pallidus neurons in both normal and parkinsonian rats

Water-avoidance stress enhances gastric contractions in freely moving conscious rats: role of peripheral CRF receptors

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