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The brain-gut axis of fish: Rainbow trout with low and high cortisol response show innate differences in intestinal integrity and brain gene expression

Journal article
Authors Malin Rosengren
Per Ove Thörnqvist
Svante Winberg
Kristina Sundell
Published in General and Comparative Endocrinology
Volume 257
Pages 235-245
ISSN 00166480
Publication year 2018
Published at Department of Biological and Environmental Sciences
Pages 235-245
Language en
Keywords Corticoid receptors, HPI-axis reactivity, Intestinal barrier function, Serotonin, Stress coping styles, Telencephalon
Subject categories Basic Medicine, Biological Sciences


© 2017 Elsevier Inc. In fish, the stress hormone cortisol is released through the action of the hypothalamic pituitary interrenal axis (HPI-axis). The reactivity of this axis differs between individuals and previous studies have linked this to different behavioural characteristics and stress coping styles. In the current study, low and high responding (LR and HR) rainbow trout in terms of cortisol release during stress were identified, using a repeated confinements stress test. The expression of stress related genes in the forebrain and the integrity of the stress sensitive primary barrier of the intestine was examined. The HR trout displayed higher expression levels of mineralocorticoid and serotonergic receptors and serotonergic re-uptake pumps in the telencephalon during both basal and stressed conditions. This confirms that HPI-axis reactivity is linked also to other neuronal behavioural modulators, as both the serotonergic and the corticoid system in the telencephalon are involved in behavioural reactivity and cognitive processes. Involvement of the HPI-axis in the brain-gut-axis was also found. LR trout displayed a lower integrity in the primary barrier of the intestine during basal conditions compared to the HR trout. However, following stress exposure, LR trout showed an unexpected increase in intestinal integrity whereas the HR trout instead suffered a reduction. This could make the LR individuals more susceptible to pathogens during basal conditions where instead HR individuals would be more vulnerable during stressed conditions. We hypothesize that these barrier differences are caused by regulation/effects on tight junction proteins possibly controlled by secondary effects of cortisol on the intestinal immune barrier or differences in parasympathetic reactivity.

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