Stimulation by interleukin-1 (IL-1) of the release of rat corticotropin-releasing factor (CRF), which is independent of the cholinergic mechanism, from superfused rat hypothalamo-neurohypophysial complexes

Ohgo, Shozo; Nakatsuru, Kuninobu; Osuga, Yutaka; Ishikawa, Emi; Matsukura, Shigeru

doi:10.1016/0006-8993(91)91320-z

Cited by 23 publications

(8 citation statements)

References 37 publications

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“…Various observations suggest that IL-P may have ef fects on the hypothalamus: (a) immunoneutralization of endogenous CRH abolishes IL-1P stimulation of the HPA axis [2,3]; (b) IL-1P injection close to PVN [9] or into the median eminence [36] activates CRH secretion in pushpull cannulated rats; (c) IL-lp perifusion of the hypothala mus [7,8,37] increases the release of CRH, and (d) IL-ip receptors have been demonstrated in the hypothalamus [38]. CRH41 is therefore an essential component of IL lp-induced activation of the HPA axis.…”

Section: Discussionmentioning

confidence: 99%

Lesions of the Afferent Catecholaminergic Pathways Inhibit the Temporal Activation of the CRH and POMC Gene Expression and ACTH Release Induced by Human Interleukin-1β in the Male Rat

et al. 1995

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A number of recent studies have suggested that interleukin-1β (IL-1β) is a major mediator contributing to the recruitment of the hypothalamo-pituitary-adrenal (HPA) axis following infectious aggressions. Central catecholamines modulate the response of the HPA axis. To investigate the importance of the afferent catecholaminergic pathways in a pathophysiological situation, we used the intraperitoneal (i.p.) IL-1β injection (mimicking peripheral infections) and we investigated the effects on the HPA responses to IL-1β of bilateral neurotoxic (6-OHDA) deletion of the ventral noradrenergic ascending bundle (VNAB-X). The VNAB is an essential stimulating pathway linking the brainstem and the paraventricular nucleus (PVN). We determined the time courses of a number of HPA variables up to 240 min after i.p. injection of IL-1β. We followed: plasma ACTH and corticosterone (CORT) concentrations, AP POMC nuclear primary RNA transcripts, AP POMC nuclear intermediate transcript RNA, AP POMC cytoplasmic mRNA, and hypothalamus (HT) CRH cytoplasmic mRNA. Compared to sham-lesioned male rats, VNAB-X animals displayed: (1) a reduced increase in plasma ACTH, and to a lesser extent in CORT throughout the experimental period with a 85% inhibition at the peak (90 min); (2) an increase in AP POMC primary nuclear transcript and in AP POMC nuclear intermediate transcript RNAs which last 60 min, instead of sustained significantly higher levels up to 240 min; (3) a similar, although reduced inhibition in the corresponding POMC cytoplasmic mRNA; (4) an almost complete abolishment of the marked biphasic rise in HT CRH mRNA. In conclusion, activation of the HPA axis by peritoneal IL-1β challenge involves CRH-producing neurons, and afferent catecholaminergic innervation of the PVN plays a crucial role in the signaling machinery linking the peritoneal aggression to the HPA axis.

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Section: Discussionmentioning

confidence: 99%

Lesions of the Afferent Catecholaminergic Pathways Inhibit the Temporal Activation of the CRH and POMC Gene Expression and ACTH Release Induced by Human Interleukin-1β in the Male Rat

et al. 1995

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“…IL-1 is known to potently stimulate CRH release in the brain to mediate several behavioral and physiological changes that follow IL-1 administration [41][42][43][44]57]. Since the LC is thought to receive CRH input [81,82], it was of interest to determine if CRH was involved in effects observed after IL-1 microinjection into the LC.…”

Section: Involvement Of Crh In Effects Of Microinjected Il-1mentioning

confidence: 99%

“…Interestingly, microinjection of a very low dose of IL-1 (5 pg) into the LC was observed to decrease, rather than increase, LC activity, and this effect (1) was specific to microinjection into the LC and (2) could also be reversed by microinfusion of IL-1RA into the LC. Because one effect of IL-1 in the brain is to stimulate the release of corticotropinreleasing hormone (CRH) [41][42][43][44], and because previous studies from our laboratory and others have found that microinjection of CRH into the LC can inhibit spontaneous activity of LC neurons [45][46][47], the possibility was tested that the inhibition of LC activity produced by 5 pg of IL-1 was mediated by IL-1-stimulated release of CRH.…”

Section: Introductionmentioning

confidence: 99%

Alteration of Locus coeruleus Neuronal Activity by Interleukin-1 and the Involvement of Endogenous Corticotropin-Releasing Hormone

Borsody

Weiss

2002

Neuroimmunomodulation

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Activity of the locus coeruleus (LC), which is the source of most of the norepinephrine in the brain, may participate in effects of the cytokine interleukin (IL)-1. This report describes the influence of IL-1β on the electrophysiological single-unit activity of LC neurons. When microinjected into the LC, human recombinant IL-1β (50 pg to 5 ng) increased the activity of LC neurons, predominantly by increasing ‘burst’ firing, which occurs in response to a sensory stimulus. At the higher doses and/or with longer time delays after injection, the spontaneous depolarization rate was also increased. This excitation (1) did not occur if IL-1β was microinjected nearby but outside of the LC and (2) could be reversed by administration of IL-1 receptor antagonist (IL-1RA). In contrast to excitatory effects, microinjection of a very low dose of IL-1β (5 pg) into the LC inhibited LC activity, and this change could also be blocked by IL-1RA. In view of earlier findings that (1) LC electrophysiological activity could be inhibited by microinjection of corticotropin-releasing hormone (CRH) into the LC region and (2) IL-1β in the brain stimulates the release of CRH, the hypothesis was tested that the inhibition of LC activity produced by the low dose of IL-1 was mediated by CRH. Microinfusion of the CRH receptor antagonist α-helical CRH(9–41) blocked the inhibition of LC activity otherwise produced by 5 pg of IL-1β, thus indicating that IL-1β also influences the activity of LC neurons via CRH. Finally, microinjection of IL-1RA alone was found to decrease LC activity, raising the possibility that LC neurons are under the influence of tonic excitation by IL-1 in the brain. In summary, the findings described here show that the activity of LC neurons can be influenced by IL-1β through stimulation of IL-1β receptors. The potential involvement of IL-1β in stress responses by means of this cytokine influencing the activity of LC neurons is discussed.

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“…Recently, several studies have shown that IL-1 is also peripheral lipopolysaccharide (LPS) injection leads to an increase in serum ACTH levels [7][8][9], IL-1 stimulation of the HPA axis has been shown to be effective at various levels of the axis. Direct action of IL-1 has been reported in the hypothalamus [3,4,7,[10][11][12], the pituitary [3][4][5][13][14][15] and the adrenal cortex [16,17], More recently, it has been suggested that in the central nervous system (CNS), the noradrenergic innervation of the paraventricu lar nuclei mediated the IL-1 activation of the HPA axis [18,19], Although IL-1 can modify brain functions [20,21], the precise mechanism of action of IL-1 in the CNS has not yet been elucidated. Autoradiographic studies using hu man 125I-IL-1 as a tracer have demonstrated the presence of high-affinity IL-1 receptors in mouse brain and anteri or pituitary [22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Regulation of lnterleukin-1 Receptor Expression in Mouse Brain and Pituitary by Lipopolysaccharide and Glucocorticoids

et al. 1993

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Interleukin-1 (IL-1) receptors have been characterized in mouse pituitary and brain. Previous studies have demonstrated that IL-1 receptor density is high in the dentate gyms in the hippocampus and that lipopolysaccharide (LPS) injection caused an 80% decrease in the number of hippocampal IL-1 receptors, while pituitary receptors in the anterior pituitary were unaffected. In order to investigate on the role of glucocorticoids (GC) in the control of IL-1 receptor expression in the brain and pituitary, the effect of stress, exogenous GC administration or adrenalectomy (ADX) on IL-1 receptor density was determined. Assays were achieved under basal and LPS-stimulated conditions by in situ quantitative autoradiography technique using human recombinant ¹²⁵I-IL-1α as a tracer. An increase of GC concentration in serum, following immobilization stress or dexamethasone (DEX) treatment (short and long term), did not modify, in the hippocampus, the density of IL-1 receptors under basal conditions or after peripheral LPS injection. On the contrary, ADX significantly decreased IL-1 receptor density in LPS-treated animals. In the anterior pituitary, a significant increase in the density of basal IL-1 receptors was observed 6 h following immobilization stress or after 7 days of DEX treatment while short-term DEX treatments are ineffective. In contrast to what was observed in the hippocampus, no changes in pituitary receptor densities were observed in ADX mice. These results indicate that hippocampal and pituitary IL-1 receptor expressions are differentially regulated by GC. Therefore, this report constitutes the first demonstration of an in vivo regulation of IL-1 receptors in the pituitary.

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Stimulation by interleukin-1 (IL-1) of the release of rat corticotropin-releasing factor (CRF), which is independent of the cholinergic mechanism, from superfused rat hypothalamo-neurohypophysial complexes

Cited by 23 publications

References 37 publications

Lesions of the Afferent Catecholaminergic Pathways Inhibit the Temporal Activation of the CRH and POMC Gene Expression and ACTH Release Induced by Human Interleukin-1β in the Male Rat

Lesions of the Afferent Catecholaminergic Pathways Inhibit the Temporal Activation of the CRH and POMC Gene Expression and ACTH Release Induced by Human Interleukin-1β in the Male Rat

Alteration of Locus coeruleus Neuronal Activity by Interleukin-1 and the Involvement of Endogenous Corticotropin-Releasing Hormone

Regulation of lnterleukin-1 Receptor Expression in Mouse Brain and Pituitary by Lipopolysaccharide and Glucocorticoids

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