scholarly journals Analysis of mechanism underlying benzamides-stimulated motor activity of dog small intestine by in vivo microdialysis

1998 ◽  
Vol 76 ◽  
pp. 295
Author(s):  
Masayuki Ogishima ◽  
Shukei Kan ◽  
Muneshige Kaibara ◽  
Kohtaro Taniyama
Keyword(s):  
Small Intestine ◽  
Motor Activity ◽  
In Vivo Microdialysis

In vivo changes in the intestinal reflexes and the response to CCK in the inflamed small intestine of the rat

2000 ◽  
Vol 279 (3) ◽  
pp. G543-G551 ◽  
Author(s):  
D. Torrents ◽  
P. Vergara
Keyword(s):  
Small Intestine ◽  
Motor Activity ◽  
Intestinal Inflammation ◽  
Trichinella Spiralis ◽  
Motor Responses ◽  
Morphological Alterations ◽  
Functional Changes ◽  
Residual Response ◽  
Abnormal Motor

Functional motor changes and morphological alterations have been associated with intestinal inflammation. The aim of our study was to evaluate functional alterations of intestinal reflexes and of the responses to CCK in the Trichinella spiralis model of intestinal inflammation. Rats were prepared with strain gauges and electrodes in the small intestine to evaluate spontaneous motor activity, the ascending contraction of the peristaltic reflex, and the motor responses to CCK-8 infusion. Infected animals showed increased motor activity at the duodenum and jejunum but not at the ileum. Ascending contraction was increased in both duodenum and ileum. Ascending excitation after Nω-nitro-l-arginine was still increased as well as the residual response after atropine. Response to CCK-8 during intestinal inflammation was changed in the jejunum, in which it turned from the inhibition shown in healthy animals to excitation. NADPH-diaphorase staining did not show any changes between distribution and density of positive neurons in either healthy or infected animals. In conclusion, intestinal inflammation induces functional changes in the motor activity that could explain the abnormal motor responses observed in inflammatory disorders.

Striatal dopamine release and metabolism in sinoaortic-denervated rats by in vivo microdialysis

1988 ◽  
Vol 254 (2) ◽  
pp. R396-R399 ◽  
Author(s):  
N. Alexander ◽  
D. Nakahara ◽  
N. Ozaki ◽  
N. Kaneda ◽  
T. Sasaoka ◽  
...  
Keyword(s):  
Motor Activity ◽  
High Performance ◽  
In Vivo Microdialysis ◽  
Striatal Dopamine ◽  
Nigrostriatal System ◽  
Electron Capture Detection ◽  
Sham Operation ◽  
Guide Tube ◽  
Microdialysis Probe

The purpose of this study was to provide new evidence favoring the hypothesis that cardiovascular information from arterial baroreceptors is integrated with the nigrostriatal system that contributes to regulation of motor activity. Samples of extracellular striatal dopamine (DA) and its metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), were collected by the technique of in vivo microdialysis and analyzed by high-performance liquid chromatography-electron capture detection. Rats were prepared with a guide tube placed in the caudate-putamen for subsequent insertion of microdialysis probes. During the 1st wk after sinoaortic denervation (SAD) or sham operation (SO), a microdialysis probe was inserted and perfused with Ringer solution at the rate of 2 microliter/min in the freely moving rats. Samples were collected every 20 min before and after injection of pargyline, 100 mg/kg ip. The results showed that SAD rats have approximately 50% less extracellular striatal DA, DOPAC, and HVA than SO rats (P less than 0.01). After blockade of monoamine oxidase activity with pargyline, striatal DA accumulated three times faster in SO than SAD rats suggesting DA synthesis is reduced in SAD rats. These data provide further evidence that the arterial baroreceptor system affects dopaminergic metabolism in the nigrostriatal system possibly as a means for integration of cardiovascular and motor activity.

Neural isolation of the entire canine stomach in vivo: effects on motility

1989 ◽  
Vol 257 (1) ◽  
pp. G30-G40 ◽  
Author(s):  
J. A. Van Lier Ribbink ◽  
M. G. Sarr ◽  
M. Tanaka
Keyword(s):  
Small Intestine ◽  
Motor Activity ◽  
Motor Pattern ◽  
Phase Iii ◽  
Myoelectric Activity ◽  
Motor Patterns ◽  
Gastric Motor Activity ◽  
Plasma Motilin ◽  
In Vivo Effects

This study was designed to determine the effects of transection of all extrinsic and enteric neural continuity to the entire stomach on motility patterns of the stomach and small intestine. Five dogs were subjected to a model of orthotopic autotransplantation of the stomach to achieve an in vivo, "neurally isolated" stomach. Manometric catheters and serosal electrodes were implanted. A cyclic motor pattern occurred during fasting and was closely coordinated temporally with the migrating motor complex (MMC) in the small bowel. The period of the cyclic gastric motor activity did not differ from the period of the MMC in the small intestine [121 +/- 8 vs 124 +/- 10 (means +/- SE) min, P = 0.4], but the periods of both were greater than in control dogs (93 +/- 5 min, P less than 0.05). Tachygastria accounted for 36 +/- 13% of fasting myoelectric activity in the neurally isolated dogs and for less than 1% in control dogs. Plasma concentration of motilin was greatest during the phase III-like gastric motor activity; exogenous motilin induced premature phase III-like activity in the stomach and small intestine. Feeding abolished the cyclic motor activity in the stomach and decreased plasma motilin concentration. These data suggest that hormonal factors, and not extrinsic or intrinsic neural continuity to the stomach, may control both the initiation of a cyclic interdigestive gastric motor pattern and its temporal coordination with motor patterns in the small intestine.

In vivo microdialysis assessment of benzamidesstimulated motor activity associated with acetyl-choline release in the dog intestine

1998 ◽  
Vol 114 ◽  
pp. A754
Author(s):  
A. Furuichi ◽  
K. Nakao ◽  
A. Enjoji ◽  
J. Furui ◽  
T. Kanematsu ◽  
...  
Keyword(s):  
Motor Activity ◽  
In Vivo Microdialysis ◽  
Acetyl Choline

scholarly journals Effects of systemic glycine on accumbal glycine and dopamine levels and ethanol intake in male Wistar rats

2020 ◽  
Author(s):  
Yasmin Olsson ◽  
Helga Höifödt Lidö ◽  
Klara Danielsson ◽  
Mia Ericson ◽  
Bo Söderpalm
Keyword(s):  
Wistar Rats ◽  
In Vivo Microdialysis ◽  
Ethanol Intake ◽  
Water Model ◽  
Glycine Transporter 1 ◽  
Improved Outcomes ◽  
Male Wistar Rats ◽  
Treatment Principle ◽  
Reward Pathway

AbstractApproved medications for alcohol use disorder (AUD) display modest effect sizes. Pharmacotherapy aimed at the mechanism(s) by which ethanol activates the dopamine reward pathway may offer improved outcomes. Basal and ethanol-induced accumbal dopamine release in the rat involve glycine receptors (GlyR) in the nucleus accumbens (nAc). Glycine transporter 1 (GlyT-1) inhibitors, which raise extracellular glycine levels, have repeatedly been shown to decrease ethanol intake in the rat. To further explore the rational for elevating glycine levels in the treatment of AUD, this study examined accumbal extracellular glycine and dopamine levels and voluntary ethanol intake and preference in the rat, after systemic treatment with glycine. The effects of three different doses of glycine i.p. on accumbal glycine and dopamine levels were examined using in vivo microdialysis in Wistar rats. In addition, the effects of the intermediate dose of glycine on voluntary ethanol intake and preference were examined in a limited access two-bottle ethanol/water model in the rat. Systemic glycine treatment increased accumbal glycine levels in a dose-related manner, whereas accumbal dopamine levels were elevated in a subpopulation of animals, defined as dopamine responders. Ethanol intake and preference decreased after systemic glycine treatment. These results give further support to the concept of elevating central glycine levels to reduce ethanol intake and indicate that targeting the glycinergic system may represent a pharmacologic treatment principle for AUD.

scholarly journals Mitochondrial transcription factor A in RORγt+ lymphocytes regulate small intestine homeostasis and metabolism

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zheng Fu ◽  
Joseph W. Dean ◽  
Lifeng Xiong ◽  
Michael W. Dougherty ◽  
Kristen N. Oliff ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Small Intestine ◽  
Th17 Cells ◽  
Tissue Remodeling ◽  
Mitochondrial Transcription ◽  
Mitochondrial Transcription Factor ◽  
Tuft Cell ◽  
Mitochondrial Transcription Factor A

AbstractRORγt+ lymphocytes, including interleukin 17 (IL-17)-producing gamma delta T (γδT17) cells, T helper 17 (Th17) cells, and group 3 innate lymphoid cells (ILC3s), are important immune regulators. Compared to Th17 cells and ILC3s, γδT17 cell metabolism and its role in tissue homeostasis remains poorly understood. Here, we report that the tissue milieu shapes splenic and intestinal γδT17 cell gene signatures. Conditional deletion of mitochondrial transcription factor A (Tfam) in RORγt+ lymphocytes significantly affects systemic γδT17 cell maintenance and reduces ILC3s without affecting Th17 cells in the gut. In vivo deletion of Tfam in RORγt+ lymphocytes, especially in γδT17 cells, results in small intestine tissue remodeling and increases small intestine length by enhancing the type 2 immune responses in mice. Moreover, these mice show dysregulation of the small intestine transcriptome and metabolism with less body weight but enhanced anti-helminth immunity. IL-22, a cytokine produced by RORγt+ lymphocytes inhibits IL-13-induced tuft cell differentiation in vitro, and suppresses the tuft cell-type 2 immune circuit and small intestine lengthening in vivo, highlighting its key role in gut tissue remodeling.

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