Plasma Hormones Facilitated the Hypermotility of the Colon in a Chronic Stress Rat Model

Liang, Chengbai; Luo, Hesheng; Liu, Ying; Cao, Jun; Xia, Hong

doi:10.1371/journal.pone.0031774

Cited by 26 publications

(23 citation statements)

References 43 publications

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“…In addition, the depression-like phenotype of PYY knockout animals [94] suggests that alterations in the expression of this gut hormone modify mood and stress coping. This contention is in line with the finding that water avoidance stress lowers the plasma level of PYY, a change that is associated with an increase in gastrointestinal motility [131].…”

Section: Effect Of Npy To Protect From the Impact Of Stress On The Gusupporting

confidence: 83%

Neuropeptides and the Microbiota-Gut-Brain Axis

Holzer

Farzi

2014

Advances in Experimental Medicine and Biology

375

290

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Neuropeptides are important mediators both within the nervous system and between neurons and other cell types. Neuropeptides such as substance P, calcitonin gene-related peptide and neuropeptide Y (NPY), vasoactive intestinal polypeptide, somatostatin and corticotropin-releasing factor are also likely to play a role in the bidirectional gut-brain communication. In this capacity they may influence the activity of the gastrointestinal microbiota and its interaction with the gutbrain axis. Current efforts in elucidating the implication of neuropeptides in the microbiota-gutbrain axis address 4 information carriers from the gut to the brain (vagal and spinal afferent neurons; immune mediators such as cytokines; gut hormones; gut microbiota-derived signalling molecules) and 4 information carriers from the central nervous system to the gut (sympathetic efferent neurons; parasympathetic efferent neurons; neuroendocrine factors involving the adrenal medulla; neuroendocrine factors involving the adrenal cortex). Apart from operating as neurotransmitters, many biologically active peptides also function as gut hormones. Given that neuropeptides and gut hormones target the same cell membrane receptors (typically G proteincoupled receptors), the two messenger roles often converge in the same or similar biological implications. This is exemplified by NPY and peptide YY (PYY), two members of the PP-fold peptide family. While PYY is almost exclusively expressed by enteroendocrine cells, NPY is found at all levels of the gut-brain and brain-gut axis. The function of PYY-releasing enteroendocrine cells is directly influenced by short chain fatty acids generated by the intestinal microbiota from indigestible fibre, while NPY may control the impact of the gut microbiota on inflammatory processes, pain, brain function and behaviour. Although the impact of neuropeptides on the interaction between the gut microbiota and brain awaits to be analysed, biologically active peptides are likely to emerge as neural and endocrine messengers in orchestrating the microbiotagut-brain axis in health and disease.

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Section: Effect Of Npy To Protect From the Impact Of Stress On The Gusupporting

confidence: 83%

Neuropeptides and the Microbiota-Gut-Brain Axis

Holzer

Farzi

2014

Advances in Experimental Medicine and Biology

375

290

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“…Exposure of rats to water avoidance stress lowers the plasma level of PYY, a change that is associated with an increase in gastrointestinal motility (Liang et al, 2012). Trinitrobenzene sulfonic acid-induced colitis increases the NPY concentration in brain and plasma (Baticic et al, 2011) whereas the expression of NPY mRNA in the brain remains unaltered by Helicobacter pylori infection (Bercik et al, 2009).…”

Section: Npy Pyy and Pp Play Specific Roles At Distinct Levels Of Thmentioning

confidence: 99%

Neuropeptide Y, peptide YY and pancreatic polypeptide in the gut–brain axis

2012

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The gut–brain axis refers to the bidirectional communication between the gut and the brain. Four information carriers (vagal and spinal afferent neurons, immune mediators such as cytokines, gut hormones and gut microbiota-derived signalling molecules) transmit information from the gut to the brain, while autonomic neurons and neuroendocrine factors carry outputs from the brain to the gut. The members of the neuropeptide Y (NPY) family of biologically active peptides, NPY, peptide YY (PYY) and pancreatic polypeptide (PP), are expressed by cell systems at distinct levels of the gut–brain axis. PYY and PP are exclusively expressed by endocrine cells of the digestive system, whereas NPY is found at all levels of the gut–brain and brain–gut axis. The major systems expressing NPY comprise enteric neurons, primary afferent neurons, several neuronal pathways throughout the brain and sympathetic neurons. In the digestive tract, NPY and PYY inhibit gastrointestinal motility and electrolyte secretion and in this way modify the input to the brain. PYY is also influenced by the intestinal microbiota, and NPY exerts, via stimulation of Y1 receptors, a proinflammatory action. Furthermore, the NPY system protects against distinct behavioural disturbances caused by peripheral immune challenge, ameliorating the acute sickness response and preventing long-term depression. At the level of the afferent system, NPY inhibits nociceptive input from the periphery to the spinal cord and brainstem. In the brain, NPY and its receptors (Y1, Y2, Y4, Y5) play important roles in regulating food intake, energy homeostasis, anxiety, mood and stress resilience. In addition, PP and PYY signal to the brain to attenuate food intake, anxiety and depression-related behaviour. These findings underscore the important role of the NPY-Y receptor system at several levels of the gut–brain axis in which NPY, PYY and PP operate both as neural and endocrine messengers.

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“…Chronic stress causes colonic hypermotility [2], [3], [4], [5], [6] and precipitates or exacerbates the symptoms of two major motility disorders, irritable bowel syndrome and inammatory bowel disease [4], [7]. The mechanisms that underline this increased colonic motility has received increased awareness in the past years.…”

Section: Introductionmentioning

confidence: 99%

Actions of Hydrogen Sulfide and ATP-Sensitive Potassium Channels on Colonic Hypermotility in a Rat Model of Chronic Stress

et al. 2013

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ObjectiveTo investigate the potential role of hydrogen sulphide (H2S) and ATP-sensitive potassium (KATP) channels in chronic stress-induced colonic hypermotility.MethodsMale Wistar rats were submitted daily to 1 h of water avoidance stress (WAS) or sham WAS (SWAS) for 10 consecutive days. Organ bath recordings, H2S production, immunohistochemistry and western blotting were performed on rat colonic samples to investigate the role of endogenous H2S in repeated WAS-induced hypermotility. Organ bath recordings and western blotting were used to detect the role of KATP channels in repeated WAS.ResultsRepeated WAS increased the number of fecal pellets per hour and the area under the curve of the spontaneous contractions of colonic strips, and decreased the endogenous production of H2S and the expression of H2S-producing enzymes in the colon devoid of mucosa and submucosa. Inhibitors of H2S-producing enzymes increased the contractile activity of colonic strips in the SWAS rats. NaHS concentration-dependently inhibited the spontaneous contractions of the strips and the NaHS IC50 for the WAS rats was significantly lower than that for the SWAS rats. The inhibitory effect of NaHS was significantly reduced by glybenclamide. Repeated WAS treatment resulted in up-regulation of Kir6.1 and SUR2B of KATP channels in the colon devoid of mucosa and submucosa.ConclusionThe colonic hypermotility induced by repeated WAS may be associated with the decreased production of endogenous H2S. The increased expression of the subunits of KATP channels in colonic smooth muscle cells may be a defensive response to repeated WAS. H2S donor may have potential clinical utility in treating chronic stress- induced colonic hypermotility.

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Plasma Hormones Facilitated the Hypermotility of the Colon in a Chronic Stress Rat Model

Cited by 26 publications

References 43 publications

Neuropeptides and the Microbiota-Gut-Brain Axis

Neuropeptides and the Microbiota-Gut-Brain Axis

Neuropeptide Y, peptide YY and pancreatic polypeptide in the gut–brain axis

Actions of Hydrogen Sulfide and ATP-Sensitive Potassium Channels on Colonic Hypermotility in a Rat Model of Chronic Stress

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