ACTH and Corticosterone Secretion Following Indomethacin, in Intact, Adrenalectomized and Dexamethasone-Pretreated Male Rats

Weidenfeld, Joseph; Siegel, Richard A.; Conforti, N.; Chowers, I.

doi:10.1159/000123435

Cited by 11 publications

(6 citation statements)

References 8 publications

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“…In contrast to the findings of others [23], we did not find a stimulatory effect of Indo alone on ACTH secretion. This is probably due to the 5-fold lower dose of Indo in the present study.…”

Section: Discussioncontrasting

confidence: 99%

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: Discussioncontrasting

confidence: 99%

Histamine and Prostaglandin Interaction in the Central Regulation of ACTH Secretion

Anthonisen¹,

Knigge²,

Kjær³

et al. 1997

Neuroendocrinology

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“…Notably, also, there was a tendency that indomethacin at this time point by itself elevated corticosterone levels. This is consistent with previous reports on a stimulatory effect of this drug on the HPA axis that occurs several hours after drug administration (Weidenfeld et al, 1983). The data from pharmacological inhibition of the Cox activity were further verified in Cox-2 Ϫ/Ϫ mice (Fig.…”

Section: Cyclooxygenase Inhibition Of Lps-induced Acth and Corticostesupporting

confidence: 92%

“…As shown in Figure 3C, parecoxib further reduced the corticosterone response, in addition to the attenuation that resulted from the gene deletion. In contrast, indomethacin treatment had no significant additive effect, a finding that may be explained by its corticosterone-releasing properties (Weidenfeld et al, 1983). Although the data suggest that mPGES-1 is coupled to Cox-2 in the late immune-induced corticosterone response, they also show that other terminal enzymes, in addition to mPGES-1, may play a role.…”

Section: Lps-induced Acth and Corticosterone Release In Mpges-1mentioning

confidence: 68%

Inducible Prostaglandin E₂Synthesis Interacts in a Temporally Supplementary Sequence with Constitutive Prostaglandin-Synthesizing Enzymes in Creating the Hypothalamic–Pituitary–Adrenal Axis Response to Immune Challenge

Elander¹,

Engström²,

Ruud³

et al. 2009

J. Neurosci.

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Inflammation-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis has been suggested to depend on prostaglandins, but the prostaglandin species and the prostaglandin-synthesizing enzymes that are responsible have not been fully identified. Here, we examined HPA axis activation in mice after genetic deletion or pharmacological inhibition of prostaglandin E 2 -synthesizing enzymes, including cyclooxygenase-1 (Cox-1), Cox-2, and microsomal prostaglandin E synthase-1 (mPGES-1). After immune challenge by intraperitoneal injection of lipopolysaccharide, the rapid stress hormone responses were intact after Cox-2 inhibition and unaffected by mPGES-1 deletion, whereas unselective Cox inhibition blunted these responses, implying the involvement of Cox-1. However, mPGES-1-deficient mice showed attenuated transcriptional activation of corticotropin-releasing hormone (CRH) that was followed by attenuated plasma concentrations of adrenocorticotropic hormone and corticosterone. Cox-2 inhibition similarly blunted the delayed corticosterone response and further attenuated corticosterone release in mPGES-1 knock-out mice. The expression of the c-fos gene, an index of synaptic activation, was maintained in the paraventricular hypothalamic nucleus and its brainstem afferents both after unselective and Cox-2 selective inhibition as well as in Cox-1, Cox-2, and mPGES-1 knock-out mice. These findings point to a mechanism by which (1) neuronal afferent signaling via brainstem autonomic relay nuclei and downstream Cox-1-dependent prostaglandin release and (2) humoral, CRH transcription-dependent signaling through induced Cox-2 and mPGES-1 elicited PGE 2 synthesis, shown to occur in brain vascular cells, play distinct, but temporally supplementary roles for the stress hormone response to inflammation.

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“…The findings also indicate that the effect of the dexamethasone in the present study was not due to an influence on sensitivity to the footshock: Dexamethasone did not significantly affect retention of animals given posttraining saline and did not affect flinch or jump thresholds. Since the dose of dexamethasone used was greater than that required for the suppression of both basal levels and stimulated release of ACTH (Weidenfeld, Siegel, Conforti, & Chowers, 1983), these findings strongly suggest that the memoryenhancing effect of epinephrine is not mediated by ACTH released from the pituitary. Although it remains to be determined whether the effects of other hormones on memory are mediated by the release of ACTH, the present findings indicate that the release of ACTH is not the common mediator of the memory-modulating effects of endogenous hormones that are known to stimulate ACTH release.…”

Section: Discussionmentioning

confidence: 85%

Memory-enhancing effect of posttraining epinephrine is not blocked by dexamethasone

et al. 1987

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There is extensive evidence that stress-related honnones administered shortly before or after training on a variety oftasks can influence retention (de Wied, 1984;McGaugh, 1983). Such evidence suggests that hormones released by learning experiences may serve as endogenous modulators of memory storage (Gold & McGaugh, 1984).Recently, Tilders, Berkenbosch, Vermes, Linton, & Smelik (1985) reported that a number of honnones, in addition to corticotrophin releasing factor (CRF) , induce the release of adrenocorticotropic honnone (ACTH) from the pituitary cortex in vitro. The hormones found to release ACTH include epinephrine, norepinephrine, arginine vasopressin, oxytocin, angiotensin 11, vasoactive intestine polypeptide (VIP), and histidine isoleucinamide. Since several of these honnones have been found to influence memory, these findings suggest that a common action by which the honnones affect memory storage might involve the release of ACTH from the anterior pituitary.Many studies have shown that posttraining administration of epinephrine alters retention: Low doses generally enhance retention, whereas high doses impair retention (McGaugh, 1983; McGaugh & Gold, in press). Epinephrine is known to stimulate the release of ACTH in vivo (Berkenbosch, Vennes, Binnekade, & Tilders, 1981;Reisine, Heisler, Hook, & Axelrod, 1983; Tilders, Berkenbosch, & Smelik, 1982) as weH as in vitro. Epinephrine is released from the adrenal medulla and is a ligand for both Q(-and ß-receptors in the periphery. Available evidence indicates that epinephrine crosses the blood-brain baITier poorly, if at a1l (Weil-Malharbe, Axelrod, & Tomchick, 1959). The effects of epinephrine on retention are blocked by a variety of Q(-and ß-adrenoreceptor antagonists (Sternberg, Korol, Novack, & McGaugh, 1986). Considered together, such findings suggest that epinephrine may influence memory storage through effects initiated at peripheral receptors.In the present study we sought to determine whether the effect of epinephrine on memory storage is mediated

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ACTH and Corticosterone Secretion Following Indomethacin, in Intact, Adrenalectomized and Dexamethasone-Pretreated Male Rats

Cited by 11 publications

References 8 publications

Histamine and Prostaglandin Interaction in the Central Regulation of ACTH Secretion

Histamine and Prostaglandin Interaction in the Central Regulation of ACTH Secretion

Inducible Prostaglandin E₂Synthesis Interacts in a Temporally Supplementary Sequence with Constitutive Prostaglandin-Synthesizing Enzymes in Creating the Hypothalamic–Pituitary–Adrenal Axis Response to Immune Challenge

Memory-enhancing effect of posttraining epinephrine is not blocked by dexamethasone

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ACTH and Corticosterone Secretion Following Indomethacin, in Intact, Adrenalectomized and Dexamethasone-Pretreated Male Rats

Cited by 11 publications

References 8 publications

Histamine and Prostaglandin Interaction in the Central Regulation of ACTH Secretion

Histamine and Prostaglandin Interaction in the Central Regulation of ACTH Secretion

Inducible Prostaglandin E2Synthesis Interacts in a Temporally Supplementary Sequence with Constitutive Prostaglandin-Synthesizing Enzymes in Creating the Hypothalamic–Pituitary–Adrenal Axis Response to Immune Challenge

Memory-enhancing effect of posttraining epinephrine is not blocked by dexamethasone

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Inducible Prostaglandin E₂Synthesis Interacts in a Temporally Supplementary Sequence with Constitutive Prostaglandin-Synthesizing Enzymes in Creating the Hypothalamic–Pituitary–Adrenal Axis Response to Immune Challenge