Intravenous administration of interleukin-1β induces Fos-like immunoreactivity in corticotropin-releasing hormone neurons in the paraventricular hypothalamic nucleus of the rat

Veening, Jan G.; Meer, M.J.M. van der; Joosten, H.W.J.; Hermus, A.R.M.M.; Rijnkels, C. E. M.; Geeraedts, L.M.G.; Sweep, Fred C.G.J.

doi:10.1016/0891-0618(93)90013-t

Cited by 33 publications

(13 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Double-labelling studies have shown that the majority of cells in the PVN that express c-Fos in response to stressful stimuli can also express CRF [71]. The dissociation between hypothalamic C- fos and Crf mRNA expressions observed in our study may indicate that dysregulation of HPA axis induced by gastritis stress is not a result of increased excitatory neural input to the PVN, but instead depends on some direct effect of gastritis on cells intrinsic to the HPA axis.…”

Section: Discussionmentioning

confidence: 54%

Experimental gastritis leads to anxiety- and depression-like behaviors in female but not male rats

et al. 2013

View full text Add to dashboard Cite

Human and animals studies support the idea that there is a gender-related co-morbidity of pain-related and inflammatory gastrointestinal (GI) diseases with psychological disorders. This co-morbidity is the evidence for the existence of GI-brain axis which consists of immune (cytokines), neural (vagus nerve) and neuroendocrine (HPA axis) pathways. Psychological stress causes disturbances in GI physiology, such as altered GI barrier function, changes in motility and secretion, development of visceral hypersensitivity, and dysfunction of inflammatory responses. Whether GI inflammation would exert impact on psychological behavior is not well established. We examined the effect of experimental gastritis on anxiety- and depression-like behaviors in male and female Sprague–Dawley rats, and evaluated potential mechanisms of action. Gastritis was induced by adding 0.1% (w/v) iodoacetamide (IAA) to the sterile drinking water for 7 days. Sucrose preference test assessed the depression-like behavior, open field test and elevated plus maze evaluated the anxiety-like behavior. IAA treatment induced gastric inflammation in rats of either gender. No behavioral abnormality or dysfunction of GI-brain axis was observed in male rats with IAA-induced gastritis. Anxiety- and depression-like behaviors were apparent and the HPA axis was hyperactive in female rats with IAA-induced gastritis. Our results show that gastric inflammation leads to anxiety- and depression-like behaviors in female but not male rats via the neuroendocrine (HPA axis) pathway, suggesting that the GI inflammation can impair normal brain function and induce changes in psychological behavior in a gender-related manner through the GI-to-brain signaling.

show abstract

Section: Discussionmentioning

confidence: 54%

Experimental gastritis leads to anxiety- and depression-like behaviors in female but not male rats

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Mascarucci et al [53] showed that ip hIL-1β (4 μg/rat ip) increased apparent glutamate release from the nucleus tractus solitarius (NTS), although heat-treated IL-1 also elicited a partial response. [54][55][56]. The structure most markedly affected is the hypothalamic PVN, which contains the cell bodies of the neurons that synthesize CRF involved in the activation of the HPA axis.…”

Section: Effects On Other Neurotransmitters-il-1βmentioning

confidence: 99%

Effects of cytokines and infections on brain neurochemistry

Dunn

2006

Clinical Neuroscience Research

281

169

View full text Add to dashboard Cite

Administration of cytokines to animals can elicit many effects on the brain, particularly neuroendocrine and behavioral effects. Cytokine administration also alters neurotransmission, which may underlie these effects. The most well studied effect is the activation of the hypothalamopituitary-adrenocortical (HPA) axis, especially that by interleukin-1 (IL-1). Peripheral and central administration of IL-1 also induces norepinephrine (NE) release in the brain, most markedly in the hypothalamus. Small changes in brain dopamine (DA) are occasionally observed, but these effects are not regionally selective. IL-1 also increases brain concentrations of tryptophan, and the metabolism of serotonin (5-HT) throughout the brain in a regionally nonselective manner. Increases of tryptophan and 5-HT, but not NE, are also elicited by IL-6, which also activates the HPA axis, although it is much less potent in these respects than IL-1. IL-2 has modest effects on DA, NE and 5-HT. Like IL-6, tumor necrosis factor-α (TNFα) activates the HPA axis, but affects NE and tryptophan only at high doses. The interferons (IFN's) induce fever and HPA axis activation in man, but such effects are weak or absent in rodents. The reported effects of IFN's on brain catecholamines and serotonin have been very varied. However, interferon-γ, and to a lesser extent, interferon-α, have profound effects on the catabolism of tryptophan, effectively reducing its concentration in plasma, and may thus limit brain 5-HT synthesis.Administration of endotoxin (LPS) elicits responses similar to those of IL-1. Bacterial and viral infections induce HPA activation, and also increase brain NE and 5-HT metabolism and brain tryptophan. Typically, there is also behavioral depression. These effects are strikingly similar to those of IL-1, suggesting that IL-1 secretion, which accompanies many infections, may mediate these responses. Studies with IL-1 antagonists, support this possibility, although in most cases the antagonism is incomplete, suggesting the existence of multiple mechanisms. Because LPS is known to stimulate the secretion of IL-1, IL-6 and TNFα, it seems likely that these cytokines mediate at least some of the responses, but studies with antagonists indicate that there are multiple mechanisms. The neurochemical responses to cytokines are likely to underlie the endocrine and behavioral responses. The NE response to IL-1 appears to be instrumental in the HPA activation, but other mechanisms exist. Neither the noradrenergic nor the serotonergic systems appear to be involved in the major behavioral responses. The significance of the serotonin response is unknown.

show abstract

“…Peripheral administration of IL-1 increased the expression of Fos protein in a number of brain regions (Chang et al, 1993;Veening et al, 1993;Ericsson et al, 1994). The structure most markedly affected is the hypothalamic PVN, which contains the cell bodies of the neurons that synthesize corticotropin-releasing factor (CRF) involved in the activation of the HPA axis.…”

Section: Other Neurochemical Responsesmentioning

confidence: 99%

Effects of the Immune System on Brain Neurochemistry

Dunn¹

2008

Handbook of Neurochemistry and Molecular Neurobiology

View full text Add to dashboard Cite

Intravenous administration of interleukin-1β induces Fos-like immunoreactivity in corticotropin-releasing hormone neurons in the paraventricular hypothalamic nucleus of the rat

Cited by 33 publications

References 30 publications

Experimental gastritis leads to anxiety- and depression-like behaviors in female but not male rats

Experimental gastritis leads to anxiety- and depression-like behaviors in female but not male rats

Effects of cytokines and infections on brain neurochemistry

Effects of the Immune System on Brain Neurochemistry

Contact Info

Product

Resources

About