Individual Behavioral Characteristics of Wild-Type Rats Predict Susceptibility to Experimental Autoimmune Encephalomyelitis

Kavelaars, Annemieke; Heijnen, Cobi J.; Tennekes, Ruth; Bruggink, J.E.; Koolhaas, Jaap M.

doi:10.1006/brbi.1998.0534

Cited by 51 publications

(24 citation statements)

References 25 publications

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“…In another behavioural study it was demonstrated that the latency of an animal to attack an intruder was inversely correlated with the disease score in EAE. Animals that did not attack an intruder were more resistant to the disease (Kavelaars et al 1999). Together, these data suggest a link between behavioural characteristics of an individual and subsequent disease severity.…”

Section: Figurementioning

confidence: 70%

Neuroendocrine Function and Chronic Inflammatory Stress

Harbuz

2002

Experimental Physiology

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The HPA axis and the response to acute stress The end-point of the activation of the HPA axis is the release of glucocorticoids (cortisol in man, corticosterone in rodents) from the adrenal cortex into the general circulation. The synthesis and release of glucocorticoids are controlled by ACTH released from the anterior pituitary gland. ACTH is synthesised from the precursor proopiomelanocortin (POMC) mRNA. The release of ACTH is regulated by the corticotrophin releasing factors corticotrophin-releasing factor(1-41) (CRF) and arginine vasopressin (AVP), which are released from the median eminence and synthesised in the parvocellular cells of the paraventricular nucleus (PVN). Under normal conditions approximately 50 % of these CRF neurons contain AVP; the remainder contain CRF but no vasopressin. CRF and AVP exert a synergistic action on the release of ACTH. The PVN acts as a co-ordinating centre receiving signals from many brain areas to regulate the response to stress. The glucocorticoids are able to regulate their own synthesis by negative feedback mediated by two corticosteroid receptors, the type II (glucocorticoid) receptor, which is found in the pituitary, PVN and other brain areas such as the hippocampus, and the type I receptor, which is found in the hippocampus. The hippocampus has a tonic inhibitory input to the PVN. In response to acute stress, the HPA axis is activated evoking the release of CRF and AVP into the The factors regulating susceptibility and severity of autoimmune diseases are poorly understood. That neuroendocrine factors are critical modulators in this regard is self-evident. For example, there are major gender differences in susceptibility with women at greater risk than men of, for example, rheumatoid arthritis (RA) and multiple sclerosis (MS). The hypothalamo-pituitary-adrenal (HPA) axis has rightly attracted a considerable amount of attention. Of particular interest has been the hypothesis that susceptibility to autoimmune disease may be related to an impaired responsiveness of the HPA axis; that is, an inability to mount an appropriate cortisol response with which to down-regulate the immune system might allow the immune system to rampage unchecked and attack self. This hypothesis links regulation of the release from the adrenal gland of the potent anti-inflammatory glucocorticoids to the disease process. Endogenous glucocorticoids are crucial for the regulation of the severity of the disease process. The hypothesis proposing a link between a hyporesponsive HPA axis and susceptibility to disease is compelling. However, evidence from a number of sources has suggested that this may not be the entire story and alterations in the activity of the HPA axis have not been consistently observed in patients with RA. This review will concentrate on recent findings concerning the HPA axis in determining susceptibility to, and in regulating the severity of, inflammatory processes in autoimmune disease. These studies have revealed that a single exposure to endotoxin can confer protection to sub...

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Section: Figurementioning

confidence: 70%

Neuroendocrine Function and Chronic Inflammatory Stress

Harbuz

2002

Experimental Physiology

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“…Although the mouse is one of the most widely used mammalian species in laboratory-based research, studies are usually conducted on inbred strains or otherwise genetically modified animals, with little information available on the "baseline", naturally evolved ancestor (see discussions in: Kavelaars, Heijnen, Tennekes, Bruggink, & Koolhaas, 1999;Koolhaas, 2008;Rangassamy et al, 2016). The study was carried out in house mice M. musculus domesticus of wild origin.…”

Section: Introductionmentioning

confidence: 99%

Individual differences in early body mass affect thermogenic performance and sibling interactions in litter huddles of the house mouse

Zepeda

Bautista

Rangassamy

et al. 2018

Developmental Psychobiology

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We asked whether within-litter differences in early body mass are associated with differences in house mouse pups' thermogenic performance and whether such variation predicts individual differences in competitive interactions for thermally more advantageous positions in the huddle. We explored pups' thermogenic performance in isolation by measuring changes in (maximal) peripheral body temperatures during a 5-min thermal challenge using infrared thermography. Changes in peripheral body temperature were significantly explained by individual differences in body mass within a litter; relatively lighter individuals showed an overall quicker temperature decrease leading to lower body temperatures toward the end of the thermal challenge compared to heavier littermates. Within the litter huddle, relatively lighter pups with a lower thermogenic performance showed consistently more rooting and climbing behavior, apparently to reach the thermally advantageous center of the huddle. This suggests that within-litter variation in starting body mass affects the pups' thermal and behavioral responses to environmental challenges.

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“…Finally, it was demonstrated that proactive coping male rats are more vulnerable for the experimental induction of the autoimmune disease experimental allergic encephalomyelitis (EAE), which is considered to be an animal model for multiple sclerosis in humans. This high vulnerability seems to be due to the high sympathetic reactivity in the proactive coping males (Kavelaars, Heijnen, Tennekes, Bruggink, & Koolhaas, 1999).…”

Section: Immunologic Defensementioning

confidence: 99%