Rat hypothalamic corticotropin-releasing hormone secretion is stimulated by interleukin-1 in an eicosanoid-dependent manner

Bernardini, Renato; Mauceri, G.; Chiarenza, Andrea

doi:10.1016/s1043-6618(09)80030-3

Cited by 12 publications

(13 citation statements)

References 2 publications

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“…and PGFju stimulated ACTH secretion, which is in accordance with previous results [4,7,8,[18][19][20][21][22], In the present experi ments PGE] and PGEiu seemed to be more potent than PGEj. As PGE2 has previously been found to be potent stimulator of ACTH secretion the present finding is diffi cult to explain.…”

Section: Discussionsupporting

confidence: 94%

“…These may likely be CRH neurons in the PVN and/ or CRH nerve terminals in the median eminence. Several studies have indicated that PGs stimulate the release of CRH and that blockade of PG synthesis inhibits the cyto kine-induced release of CRH [2,3,8,10,12,15,24], and it has been demonstrated that HA increases ACTH secre tion by stimulation of CRH synthesis and release [36][37][38][39][40]. Furthermore, it has recently been reported that Indo as well as an H] but not an H: receptor antagonist inhibited LPS-induced formation of c-Jos protein (an indicator of neuronal activation) in the PVN [14], Therefore, it is sug gested that endogenous PGs by activation of CRH neu rons contribute to HA-induced stimulation of the HPA axis and that the PGE|/PGF2a-stimulated ACTH secre tion depends on activation of CRH neurons via stimula tion of histaminergic H| receptors, which are present in the PVN [42].…”

Section: Discussionmentioning

confidence: 99%

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Histamine and Prostaglandin Interaction in the Central Regulation of ACTH Secretion

Anthonisen¹,

Knigge²,

Kjær³

et al. 1997

Neuroendocrinology

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Since prostaglandins (PGs) and histamine (HA) seem to be involved in the activation of the hypothalamic-pituitary-adrenal axis following immunochallenges with lipopolysaccharide (LPS) endotoxin and cytokines, we investigated whether the histaminergic and eicosanoid systems in the male rat brain interact in their regulation of ACTH secretion. The PG synthesis inhibitor indomethacin (10 mg/kg i.p.) attenuated the ACTH response to LPS (10 µg/kg i.p.) and HA (30 µg i.c.v.). Infusion of PGE₁, PGE₂ or PGF_2α (1 and/or 5 µg infused intracerebroventricularly) stimulated ACTH secretion. The ACTH response to PGEi was inhibited by the HA synthesis inhibitor α-fluoromethyl-histidine and the H_1· receptor antagonist mepyramine (MEP) but not the H₂ receptor antagonist cimetidine (CIM). Neither MEP nor CIM affected the ACTH response to PGE₂. MEP and CIM attenuated the ACTH response induced by PGF2_α. The findings indicate that HA and some PGs in the brain interact in their stimulatory regulation of ACTH secretion. Such an interaction may also be involved in their mediation of the ACTH response to immunochallenges.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Histamine and Prostaglandin Interaction in the Central Regulation of ACTH Secretion

Anthonisen¹,

Knigge²,

Kjær³

et al. 1997

Neuroendocrinology

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“…CRH secretion has been shown to be modulated in vitro by prostanoids and platelet activating factor, in studies using rat tissues (29)(30)(31). Since the long-term use of NSAIDs by RA patients and NIAIOA controls was comparable in this study, the use of these agents and prostaglandin effects cannot explain the observed hypothalamic defect (Tables 1 and 2).…”

Section: Discussionmentioning

confidence: 63%

Defective hypothalamic response to immune and inflammatory stimuli in patients with rheumatoid arthritis

Chikanza

Petrou

Kingsley

et al. 1992

Arthritis & Rheumatism

337

163

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Objective. To determine the integrity of the hypothalamic-pituitary-adrenal (HPA) axis responses to immune/inflammatory stimuli in patients with rheumatoid arthritis (RA).Methods. Diurnal secretion of cortisol and the cytokine and cortisol responses to surgery were studied in subjects with active RA, in subjects with chronic osteomyelitis (OM), and in subjects with noninflammatory arthritis, who served as controls.Results. Patients with RA had a defective HPA response, as evidenced by a diurnal cortisol rhythm of secretion which was at the lower limit of normal in contrast to those with OM, and a failure to increase cortisol secretion following surgery, despite high levels of interleukin-Ijl (IL-lm and IL-6. The corticotropinreleasing hormone stimulation test in the RA patients showed normal results, thus suggesting a hypothalamic defect, but normal pituitary and adrenal function.Conclusion. These findings suggest that RA patients have an abnormality of the HPA axis response to

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“…may depend on prostaglan dins (PGs) in the hypothalamus. Indomethacin, an inhibi tor of PG synthesis, has been shown to block the induc tion of CRH secretion by IL-1 [3 from hypothalamic ex plants in vitro [21][22][23], as well as the ACTH response to intravenous or intracerebroventricular IL-1 [3 [5, 24. 25], The precise site of action whereby PGs mediate this inter action remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Prostaglandins Mediate the ACTH Response to lnterleukin-1-Beta Instilled into the Hypothalamic Median Eminence

1994

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Interleukin-1β (IL-1β) is a potent ACTH secretagogue which activates the release of hypothalamic CRH. Direct injections of IL-1β into the hypothalamic median eminence (ME), a site which lacks a blood-brain barrier, has been shown to rapidly induce ACTH secretion. Therefore, the ME is a likely site whereby circulating IL-1β can access the brain to stimulate CRH and, consequently, ACTH secretion. To further evaluate this hypothesis, an angular stereotaxic approach was developed to localize the spread of IL-1β to the ME and to optimally separate the injectate from the hypothalamic paraventricular nucleus (PVN), another proposed site of IL-1 action. Studies of the diffusion of [¹²⁵I]-IL-1β (100 nl delivered over 60 s) showed that 97% remained within 200 µm of the ventral surface of the hypothalamus and 87% was contained within a radius of 550 µm of the injection site in the sagittal plane. Additional rats received recombinant human IL-1β (0.2-25.0 ng in 100 nl) into the ME (intra-ME). Plasma ACTH levels were significantly elevated by a much lower dose (0.5 ng, p < 0.001) of IL-1β than that previously reported. Responses appeared to be dose-dependent and ACTH was maximally stimulated by 2.0 ng IL-1β. Also, immunocytochemically labelled CRH in the ME was markedly depleted after intra-ME IL-1β. Indomethacin, an inhibitor of prostaglandin (PG) synthesis, has been shown to block both the induction of CRH secretion by IL-lβ from hypothalamic explants, as well as the ACTH response to intravenous IL-1β. Thus, indomethacin was used to determine whether PGs are mediators of the ACTH response to IL-1β delivered into the ME. The ACTH response was abolished (p < 0.005) when a low dose of indomethacin (1 mg/kg i.v.) was administered 20 min before intra-ME IL-1β (25 ng). Finally, plasma ACTH was elevated in a dose-dependent manner by the intra-ME administration of PGs. The hierarchy of ACTH responses to PGE₂ were: CSF < 0.5 µg (p < 0.001) = 2.0 µg < 4.0 µg(p < 0.05). Responses to PGF_2α were: CSF < 0.5 µg (p < 0.001) < 2.0 µg (p < 0.05) = 4.0 µg. Since these PGs appear to activate different second-messenger systems, a submaximal dose of each was administered alone or in combination. Additivity of the response, rather than synergy, was evident, since the overall ACTH level in response to the combination of PGE₂ and PGF_2α (0.5 µg each) was no greater than the sum of the two separate treatments. In summary, the ACTH response to IL-1β delivered into the ME appears to be mediated by local prostaglandins.

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Rat hypothalamic corticotropin-releasing hormone secretion is stimulated by interleukin-1 in an eicosanoid-dependent manner

Cited by 12 publications

References 2 publications

Histamine and Prostaglandin Interaction in the Central Regulation of ACTH Secretion

Histamine and Prostaglandin Interaction in the Central Regulation of ACTH Secretion

Defective hypothalamic response to immune and inflammatory stimuli in patients with rheumatoid arthritis

Prostaglandins Mediate the ACTH Response to lnterleukin-1-Beta Instilled into the Hypothalamic Median Eminence

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