Expression and localization of p80 and p68 interleukin-1 receptor proteins in the brain of adult mice

French, Richard A.; VanHoy, Roger W.; Chizzonite, R; Zachary, James F.; Dantzer, Robert; Parnet, Patricia; Bluthé, Rose Marie; Kelley, Keith W.

doi:10.1016/s0165-5728(98)00224-0

Cited by 106 publications

(53 citation statements)

References 47 publications

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“…7 A and C). The expression pattern of IL-1RI is the same as reported (29,30). This pattern was not observed in IL-1RI null mice and was blocked by preabsorption of the IL-1RI antibody with IL-1RI-blocking peptide in rats (SI Fig.…”

Section: Effects Of Acute and Chronic Stress Are Blocked In Il-1ri Nusupporting

confidence: 77%

IL-1β is an essential mediator of the antineurogenic and anhedonic effects of stress

Koo

Duman

2008

Proc. Natl. Acad. Sci. U.S.A.

775

564

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Stress decreases neurogenesis in the adult hippocampus, and blockade of this effect is required for the actions of antidepressants in behavioral models of depression. However, the mechanisms underlying these effects of stress have not been identified. Here, we demonstrate an essential role for the proinflammatory cytokine IL-1␤. Administration of IL-1␤ or acute stress suppressed hippocampal cell proliferation. Blockade of the IL-1␤ receptor, IL-1RI, by using either an inhibitor or IL-1RI null mice blocks the antineurogenic effect of stress and blocks the anhedonic behavior caused by chronic stress exposure. In vivo and in vitro studies demonstrate that hippocampal neural progenitor cells express IL-1RI and that activation of this receptor decreases cell proliferation via the nuclear factor-B signaling pathway. These findings demonstrate that IL-1␤ is a critical mediator of the antineurogenic and depressive-like behavior caused by acute and chronic stress.cytokine ͉ depression ͉ neurogenesis T he profound consequences of stress exposure, defined as disturbances of physiological homeostasis, include a detrimental impact on certain aspects of brain function (1, 2). In particular, uncontrollable stress is a major contributing factor for neuropsychiatric disorders such as major depression and posttraumatic stress disorders (3, 4). Alterations at the cellular level in the hippocampus have been linked to the pathophysiology of stress-related mood disorders (5-7). Many studies demonstrate that stressful experiences suppress hippocampal neurogenesis, which could contribute to the hippocampal atrophy observed in depressed patients (8-10). In contrast, antidepressant treatment increases hippocampal neurogenesis, blocks the antineurogenic effects of stress (11,12), and reduces or even reverses hippocampal atrophy (9, 11). Recent studies demonstrate that new hippocampal neurons are required for the actions of antidepressants in behavioral models of depression and anxiety (13, 14) with some exceptions (15,16).Despite this progress, the mechanisms underlying the antineurogenic and behavioral actions of stress remain ill defined. One possibility is that excessive proinflammatory cytokines, particularly IL-1␤, contribute to the actions of stress. Animal studies demonstrate that exposure to stress increases IL-1␤ in several brain areas, including the hippocampus (17-20), and central administration of IL-1␤ produces several stress-like effects, including activation of the hypothalamic-pituitary-adrenal (HPA) axis (17, 21), inhibition of hippocampal long-term potentiation (22), down-regulation of hippocampal brain-derived neurotrophic factor (23), and impaired hippocampal-dependent contextual fear conditioning (24). In contrast, blockade of the receptor, IL-1RI that mediates the actions of IL-1␤ (25) inhibits these stress-like effects (23, 24) and blocks the antiproliferative effects of INF-␣ in the hippocampus (26).Based on this evidence, the current study was undertaken to test the hypothesis that the antineurogenic and depressiv...

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Section: Effects Of Acute and Chronic Stress Are Blocked In Il-1ri Nusupporting

confidence: 77%

IL-1β is an essential mediator of the antineurogenic and anhedonic effects of stress

Koo

Duman

2008

Proc. Natl. Acad. Sci. U.S.A.

775

564

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“…This suggests that the ability of IL-1β to inhibit GnRH release could be an effect of its direct action in the hypothalamus IL-1 type I receptors. The presence of IL-1 receptor type I in the CNS neurons suggests possible direct regulation of the neuroendocrine system by IL-1b (French et al, 1999). Moreover, in vitro studies showed that the IL-1 receptor is present in the membrane of immortalized GnRH neurons, the Gnv-4 cell line, which synthesize and release gonadoliberin (Igaz et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Does central IL-1β affect GnRH secretion in the hypothalamus of anoestrous ewes via different regulatory pathways?

Tomaszewska-Zaremba¹,

Herman²,

Misztal³

2013

J. Anim. Feed Sci.

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“…As described above, cerebellar Il1b expression was enhanced 5 days after subchronic THC treatment cessation in CD11b + (P4) cells, and was constantly altered in Cb1 -/-mice. Local microinjection of IL-1β into the cerebellum is known to produce ataxia (37) and to enhance the firing rates of cerebellar Purkinje neurons (38) acting on the IL-1 receptors (IL-1Rs) that are strongly expressed in Purkinje neurons (39). We therefore tested whether an inhibitor of IL-1R signaling, an end-protected L-valyl derivative with antagonistic effects on IL-1R (IL-1RA), would improve cerebellar performance under our experimental conditions.…”

Section: Figurementioning

confidence: 99%

Microglial activation underlies cerebellar deficits produced by repeated cannabis exposure

et al. 2013

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Chronic cannabis exposure can lead to cerebellar dysfunction in humans, but the neurobiological mechanisms involved remain incompletely understood. Here, we found that in mice, subchronic administration of the psychoactive component of cannabis, delta9-tetrahydrocannabinol (THC), activated cerebellar microglia and increased the expression of neuroinflammatory markers, including IL-1β. This neuroinflammatory phenotype correlated with deficits in cerebellar conditioned learning and fine motor coordination. The neuroinflammatory phenotype was readily detectable in the cerebellum of mice with global loss of the CB1 cannabinoid receptor (CB1R, Cb1 -/-mice) and in mice lacking CB1R in the cerebellar parallel fibers, suggesting that CB1R downregulation in the cerebellar molecular layer plays a key role in THC-induced cerebellar deficits. Expression of CB2 cannabinoid receptor (CB2R) and Il1b mRNA was increased under neuroinflammatory conditions in activated CD11b-positive microglial cells. Furthermore, administration of the immunosuppressant minocycline or an inhibitor of IL-1β receptor signaling prevented the deficits in cerebellar function in Cb1 -/-and THC-withdrawn mice. Our results suggest that cerebellar microglial activation plays a crucial role in the cerebellar deficits induced by repeated cannabis exposure.

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Expression and localization of p80 and p68 interleukin-1 receptor proteins in the brain of adult mice

Cited by 106 publications

References 47 publications

IL-1β is an essential mediator of the antineurogenic and anhedonic effects of stress

IL-1β is an essential mediator of the antineurogenic and anhedonic effects of stress

Does central IL-1β affect GnRH secretion in the hypothalamus of anoestrous ewes via different regulatory pathways?

Microglial activation underlies cerebellar deficits produced by repeated cannabis exposure

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