@article{10902/29926,
year = {2023},
url = {https://hdl.handle.net/10902/29926},
abstract = {Background/Aims
Chronic psychological stress affects gastrointestinal physiology which may underpin alterations in the immune response and epithelial transport, both functions are partly regulated by enteric nervous system. However, its effects on enteric neuroplasticity are still unclear. This study aims to investigate the effects of chronic unpredictable psychological stress on intestinal motility and prominent markers of enteric function.
Methods
Adult male C57BL/6J mice were exposed to 19 day of unpredictable stress protocol schedule of social defeat and overcrowding. We investigated the effects on plasma corticosterone, food intake, and body weight. In vivo gastrointestinal motility was assessed by fecal pellet output and by whole-gastrointestinal transit (using the carmine red method). Tissue monoamine level, neural and glial markers, neurotrophic factors, monoamine signaling, and Toll-like receptor expression in the proximal and distal colon, and terminal ileum were also assessed.
Results
Following chronic unpredictable psychological stress, stressed mice showed increased food intake and body weight gain (P < 0.001), and reduced corticosterone levels (P < 0.05) compared to control mice. Stressed mice had reduced stool output without differences in water content, and showed a delayed gastrointestinal transit compared to control mice (P < 0.05). Stressed mice exhibited decreased mRNA expression of tyrosine hydroxylase (Th), brain-derived neurotrophic factor (Bdnf) and glial cell-derived neurotrophic factor (Gdnf), as well as Toll-like receptor 2 (Tlr2) compared to control (P < 0.05), only proximal colon. These molecular changes in proximal colon were associated with higher levels of monoamines in tissue.
Conclusion
Unpredictable psychological chronic stress induces region-specific impairment in monoamine levels and neuroplasticity markers that may relate to delayed intestinal transit.},
organization = {Financial support: This study was supported in part by Fondo Europeo de Desarrollo Regional (FEDER), Fondo de Investigación Sanitaria, and Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Instituto de Salud Carlos III, Subdirección General de Investigación Sanitaria, Ministerio de Economía y Competitividad: CM08/0022 and Beca Estada l’estranger (Societat Catalana Digestología) 2011 and PI19/01643 (Beatriz Lobo); PI17/01902 (Javier Santos) CIBEREHD (Javier Santos); Vall d’Hebron Institut de Recerca. FONDECYT #1181699 and #11121527; MECESUP 0608 Universidad de Chile (Caroll Beltran). The work described herein was supported by APC Microbiome Ireland, funded by Science Foundation Ireland (SFI), through the Irish Government’s National Development Plan. The authors and their work were supported by SFI (Grant No. 02/CE/B124, 07/CE/B1368, and SFI/12/RC/2273).
Acknowledgements: We would like to thank Rachel D Moloney and Mr Patrick Fitzgerald for their technical assistance and Dr Bruno M Godinho for help with spleen stimulation studies.},
publisher = {Korean Society of Neurogastroenterology and Motility},
publisher = {Journal of Neurogastroenterology and Motility, 2023, 29, 1},
title = {The stressed gut: region-specific immune and neuroplasticity changes in response to chronic psychosocial stress},
author = {Lobo, Beatriz and Tramullas Fernández, Mónica and Finger, Beate-C and Lomasney, Kevin W. and Beltran, Caroll and Clarke, Gerard and Santos, Javier and Hyland, Niall P. and Dinan, Timothy G. and Cryan, John F.},
}