Oxytocin is expressed by both intrinsic sensory and secretomotor neurons in the enteric nervous system of guinea pig

Yu, Qiang; Ji, Ruihua; Gao, Xiaofei; Fu, Jiqiang; Guo, Wei; Song, Xianmin; Zhang, Xiaolin; Burnstock, Geoffrey; Shi, Xueyin; He, Cheng; Xiang, Zhenghua

doi:10.1007/s00441-011-1155-0

Cited by 21 publications

(31 citation statements)

References 18 publications

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“…Atosiban is also, for example, a vasopressin antagonist (4). The question of the species variation in the enteric actions of OT, therefore, is still an open one; nevertheless, OT and OTR do appear to be expressed, not only in the murine gut, but also in the human (34,38) and rat bowel (65).…”

Section: Discussionmentioning

confidence: 98%

Oxytocin regulates gastrointestinal motility, inflammation, macromolecular permeability, and mucosal maintenance in mice

Welch

Margolis

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

130

136

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Enteric neurons express oxytocin (OT); moreover, enteric neurons and enterocytes express developmentally regulated OT receptors (OTRs). Although OT (with secretin) opposes intestinal inflammation, physiological roles played by enteric OT/OTR signaling have not previously been determined. We tested hypotheses that OT/OTR signaling contributes to enteric nervous system (ENS)-related gastrointestinal (GI) physiology. GI functions and OT effects were compared in OTR-knockout (OTRKO) and wild-type (WT) mice. Stool mass and water content were greater in OTRKO mice than in WT. GI transit time in OTRKO animals was faster than in WT; OT inhibited in vitro generation of ENS-dependent colonic migrating motor complexes in WT but not in OTRKO mice. Myenteric neurons were hyperplastic in OTRKO animals, and mucosal exposure to cholera toxin (CTX) in vitro activated Fos in more myenteric neurons in OTRKO than WT than in WT mice; OT inhibited the CTX response in WT but not in OTRKO mice. Villi and crypts were shorter in OTRKO than in WT mice, and transit-amplifying cell proliferation in OTRKO crypts was deficient. Macromolecular intestinal permeability in OTRKO was greater than WT mice, and experimental colitis was more severe in OTRKO mice; moreover, OT protected WT animals from colitis. Observations suggest that OT/OTR signaling acts as a brake on intestinal motility, decreases mucosal activation of enteric neurons, and promotes enteric neuronal development and/or survival. It also regulates proliferation of crypt cells and mucosal permeability; moreover OT/OTR signaling is protective against inflammation. Oxytocinergic signaling thus appears to play an important role in multiple GI functions that are subject to neuronal regulation.

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Section: Discussionmentioning

confidence: 98%

Oxytocin regulates gastrointestinal motility, inflammation, macromolecular permeability, and mucosal maintenance in mice

Welch

Margolis

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

130

136

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“…Of note, conditional knockout mice in which forebrain OTRs were deleted postnatally showed reduction in body mass (45), suggesting that OT's effects on energy metabolism are mediated within the central nervous system. On the other hand, studies on OT regulation of gastric motility support both central and peripheral OT action (61,89). Likewise, several reports showed that circulating OT regulates adiposity since adipocytes express its receptors (83).…”

Section: Perspectives and Significancementioning

confidence: 98%

Oxytocin and bone

Colaianni

Sun

Zaidi

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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One of the most meaningful results recently achieved in bone research has been to reveal that the pituitary hormones have profound effect on bone, so that the pituitary-bone axis has become one of the major topics in skeletal physiology. Here, we discuss the relevant evidence about the posterior pituitary hormone oxytocin (OT), previously thought to exclusively regulate parturition and breastfeeding, which has recently been established to directly regulate bone mass. Both osteoblasts and osteoclasts express OT receptors (OTR), whose stimulation enhances bone mass. Consistent with this, mice deficient in OT or OTR display profoundly impaired bone formation. In contrast, bone resorption remains unaffected in OT deficiency because, even while OT stimulates the genesis of osteoclasts, it inhibits their resorptive function. Furthermore, in addition to its origin from the pituitary, OT is also produced by bone marrow osteoblasts acting as paracrine-autocrine regulator of bone formation modulated by estrogens. In turn, the power of estrogen to increase bone mass is OTR-dependent. Therefore, OTR(-/-) mice injected with 17β-estradiol do not show any effects on bone formation parameters, while the same treatment increases bone mass in wild-type mice. These findings together provide evidence for an anabolic action of OT in regulating bone mass and suggest that bone marrow OT may enhance the bone-forming action of estrogen through an autocrine circuit. This established new physiological role for OT in the maintenance of skeletal integrity further suggests the potential use of this hormone for the treatment of osteoporosis.

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“…When human subjects receive social stimuli, it is likely that this causes reactions in the viscera (especially heart and gut) and the heart and the gut may themselves contribute to OXT plasma levels (Yu et al, 2011). More significantly, visceral signals will be picked up by the afferent branches of the vagus nerve and other visceral afferents, and will register as emotional signals in the brain.…”

Section: Pharmacokinetics Of Oxytocin and Vasopressinmentioning

confidence: 99%

Modulating social behavior with oxytocin: How does it work? What does it mean?

Churchland

Winkielman

2012

Hormones and Behavior

404

340

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Among its many roles in body and brain, oxytocin influences social behavior. Understanding the precise nature of this influence is crucial, both within the broader theoretical context of neurobiology, social neuroscience and brain evolution, but also within a clinical context of disorders such as anxiety, schizophrenia, and autism. Research exploring oxytocin’s role in human social behavior is difficult owing to its release in both body and brain and its interactive effects with other hormones and neuromodulators. Additional difficulties are due to the intricacies of the blood-brain barrier and oxytocin’s instability, which creates measurement issues. Questions concerning how to interpret behavioral results of human experiments manipulating oxytocin are thus made all the more pressing. The current paper discusses several such questions. We highlight unresolved fundamental issues about what exactly happens when oxytocin is administered intranasally, whether such oxytocin does in fact reach appropriate receptors in brain, and whether central or peripheral influences account for the observed behavioral effects. We also highlight the deeper conceptual issue of whether the human data should be narrowly interpreted as implicating a specific role for oxytocin in complex social cognition, such a generosity, trust, or mentalizing, or more broadly interpreted as implicating a lower-level general effect on general states and dispositions, such as anxiety and social motivation. Using several influential studies, we show how seemingly specific, higher-level social-cognitive effects can emerge via a process by which oxytocin’s broad influence is channeled into a specific social behavior in a context of an appropriate social and research setting.

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Oxytocin is expressed by both intrinsic sensory and secretomotor neurons in the enteric nervous system of guinea pig

Cited by 21 publications

References 18 publications

Oxytocin regulates gastrointestinal motility, inflammation, macromolecular permeability, and mucosal maintenance in mice

Oxytocin regulates gastrointestinal motility, inflammation, macromolecular permeability, and mucosal maintenance in mice

Oxytocin and bone

Modulating social behavior with oxytocin: How does it work? What does it mean?

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