Inhibitory effect of norepinephrine on immunoreactive corticotropin-releasing factor release from the rat hypothalamus in vitro

Suda, Toshio; Yajima, Fumiko; Tomori, Naoki; Sumitomo, Takashi; Nakagami, Yuriko; Ushiyama, Tsuyako; Demura, Hiroshi; Shizume, Kazuo

doi:10.1016/0024-3205(87)90012-9

Cited by 40 publications

(18 citation statements)

References 16 publications

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“…These data also agree with those obtained from investigations of other in vitro systems [20,21,22,24], but not with those of Suda et al [25] who reported that NA inhibited CRH release from the hypothalamus in perifusion experiments. The present study also showed that CRH release increased both with increasing concentrations of NA for a fixed incubation time and increasing incubation times with a determined NA concentration.…”

Section: Discussionsupporting

confidence: 82%

“…For example, Widmaier et al [21] and Hu et al [22] used fetal hypothalamic cell cultures containing 10% fetal bovine or calf serum. Suda et al [25] placed hypothalami in perifusion chambers and used a defined perifusion medium without serum or steroids. Addition ally, all in vitro systems, and especially those using dis persed hypothalamic cells, exclude extrahypothalamic sites of corticosteroid-catecholamine interactions, e.g., in the brain stem [39] and in the limbic system [28,40] which are involved in the HPA regulation.…”

Section: Discussionmentioning

confidence: 99%

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Removal of Adrenal Steroids from the Medium Reverses the Stimulating Effect of Catecholamines on Corticotropin Releasing Hormone Neurons in Organotypic Cultures

Szafarczyk¹,

Feuvrier²,

Siaud³

et al. 1995

Neuroendocrinology

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An organotypic culture system of anterior hypothalamic slices was developed for studying the secretory responses of corticotropin-releasing hormone (CRH) neurons to corticosteroid-catecholamine interactions. The standard culture medium included 5% horse serum containing 50 µg/l cortisol. In 1- to 3-day cultures, the tissue viability was demonstrated by the presence of arginine vasopressin immunolabeled perikarya and axons in the paraventricular nucleus and by sustained tissue concentrations of CRH (around 50 pg/mg protein). However, immunoreactive CRH neurons were not detectable in cultures in the standard medium. Exposure of cultures to high K⁺ (56 mM) in the medium induced a ten-fold increase in basal CRH release which was completely abolished in a Ca²⁺-free medium containing 2 mMEGTA. Noradrenaline (NA) triggered CRH release in a dose-dependent (1-20 µM) and time-dependent (0.5-6 h) manner. Removal of corticosteroids from the media by charcoal treatment led to (1) the visualization of immunolabelled CRH perikarya and fibers and a 55 % rise in CRH content of the paraventricular nucleus tissue and (2) to a five-fold increase in CRH release. Both effects were reversed by supplementation of the culture medium with corticosterone (50 µg/l). Under steroid-free conditions, NA (1–10 µM) not only failed to induce CRH release, but strongly inhibited the consistent baseline in CRH release. This was reminiscent of a similar corticosteroid-dependent inversion of the NA effect on the hypothalamic-pituitary-adrenal axis described in vivo. Overall, these results are direct evidence of complex corticosteroid-catecholamine interrelationships as major regulatory factors of the hypothalamic-pituitary-adrenal axis.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Removal of Adrenal Steroids from the Medium Reverses the Stimulating Effect of Catecholamines on Corticotropin Releasing Hormone Neurons in Organotypic Cultures

Szafarczyk¹,

Feuvrier²,

Siaud³

et al. 1995

Neuroendocrinology

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“…This stimulatory effect of NE on CRF release has been observed in rat hypothalamic explants and was blocked by beta-adrenergic receptor antagonists, but not alpha adrenergic receptor blocking drugs (Tsagarakis et al, 1988). However, others (Suda et al, 1987) have reported decreased release of hypothalamic CRF after incubation of isolated hypothalamus with nanomolar concentrations of NE that were blocked by both alpha-and beta-adrenergic antagonists. Destruction of noradrenergic efferents to the hypothalamus with a neurotoxin such as 6-hydroxy dopamine (Feldman and Weidenfeld, 1993) or brain-stem hemisection (Pacak et al, 1993) attenuates activation of the HPA axis by stressors such as bright light, loud noise, and immobilization.…”

Section: Discussionmentioning

confidence: 71%

Elevated Concentrations of CRF in the Locus Coeruleus of Depressed Subjects

Bissette

Klimek

Pan

et al. 2003

Neuropsychopharmacol

132

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Research evidence that corticotropin-releasing factor (CRF) plays a role in the pathophysiology of major depressive disorder (MDD) has accumulated over the past 20 years. The elevation of lumbar cerebrospinal fluid (CSF) concentrations of CRF decreased responsiveness of pituitary CRF receptors to challenge with synthetic CRF, and increased levels of serum cortisol in MDD subjects support the hypothesis that CRF is chronically hypersecreted in at least the endocrine circuits of the hypothalamic-pituitary-adrenal (HPA) axis and may also involve other CRF brain circuits mediating emotional responses and/or arousal. One such circuit includes the excitatory CRF input to the locus coeruleus (LC), the major source of norepinephrine in the brain. Furthermore, there are now reports of decreased levels of CRF in lumbar CSF from MDD patients after symptom relief from chronic treatment with antidepressant drugs or electroconvulsive therapy. Whether this normalization reflects therapeutic effects on both endocrine-and limbic-associated CRF circuits has not yet been effectively addressed. In this brief report, we describe increased concentrations of CRF-like immunoreactivity in micropunches of post-mortem LC from subjects with MDD symptoms as established by retrospective psychiatric diagnosis compared to nondepressed subjects matched for age and sex.

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“…A number of known inputs to the CRH neurosecretory sys tem need to be investigated concerning possible differ ential effects on peptide expression in the two subpopula tions [4], The elevation of neurosecretory vesicle content in CRH+/VP-axons after the high dose of methoxamine was unexpected; this was presumably due to inhibition of baseline activity of these axons. Inhibition of CRH release during a r adrenergic activation has been observed in an in vitro preparation [42], but not during stress [8]. The mechanism of inhibiting the CRH+/VP-subpopulation is unknown; methoxamine-induced elevations in circulat ing corticosterone do not offer a simple explanation, since these elevations were higher after the lower dose, and inhibition of the CRH+/VP-subpopulation was not ob served after this dose.…”

Section: Discussionmentioning

confidence: 85%

Contrasting Effects of Central Alpha-1-Adrenoreceptor Activation on Stress-Responsive and Stress-Nonresponsive Subpopulations of Corticotropin-Releasing Hormone Neurosecretory Cells in the Rat

Whitnall¹,

Kiss

Aguilera

1993

Neuroendocrinology

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Stimulation of the rat hypothalamopituitary-adrenal axis during stress involves activation of central α₁-adrenergic receptors. The subpopulation of corticotropin-releasing hormone (CRH) neurosecretory cells that contains vasopressin (VP) is selectively activated by several types of stress (immobilization, hypoglycemia, and intracerebroventricular, i.c.v., colchicine), and is located in a catecholamine-rich area of the hypothalamic paraventricular nucleus. Therefore, we tested the hypothesis that the CRH+/VP+ subpopulation is selectively activated by central α₁-adrenergic receptors. The α₁-agonist methoxamine or vehicle alone was injected i.c.v. after habituation of rats to daily injections of vehicle through a chronic i.c.v. cannula. Activation of the CRH+/VP+ and CRH+/VP-subpopulations was measured by quantifying depletion of neurosecretory vesicles from immunocytochemically identified axons in the external zone of the median eminence. The habituated, vehicle-injected sham control group had normal levels of plasma ACTH and corticosterone, but possessed a significantly higher proportion of VP-containing CRH axons than naive animals. This change is similar to what was observed previously in rats subjected to repeated daily stress. I.c.v. methoxamine caused elevations of plasma ACTH and corticosterone and significant depletions of vesicles from the CRH+/VP+ axons at 1 and 2 h after injection, compared to the sham control group. The CRH+/VP-axons, however, displayed significant accumulations of neurosecretory vesicles at the same times after 300 µg methoxamine, compared to the sham control group. After 100 µg methoxamine, there was no change in the CRH+/VP-axons, compared to the sham control group. We interpret the accumulation of vesicles in the VP-deficient CRH neurosecretory axons after 300 µg i.c.v. methoxamine to reflect inhibition of this subpopulation after central α₁-adrenergic receptor activation. The results demonstrate for the first time that central catecholamines induce release of both CRH and VP in the portal capillary plexus. These findings support the hypothesis that stress induces release of catecholamines from axons projecting to the paraventricular nucleus, thus activating α₁-adrenergic receptors that selectively stimulate the VP-containing subpopulation of CRH neurosecretory cells.

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Inhibitory effect of norepinephrine on immunoreactive corticotropin-releasing factor release from the rat hypothalamus in vitro

Cited by 40 publications

References 16 publications

Removal of Adrenal Steroids from the Medium Reverses the Stimulating Effect of Catecholamines on Corticotropin Releasing Hormone Neurons in Organotypic Cultures

Removal of Adrenal Steroids from the Medium Reverses the Stimulating Effect of Catecholamines on Corticotropin Releasing Hormone Neurons in Organotypic Cultures

Elevated Concentrations of CRF in the Locus Coeruleus of Depressed Subjects

Contrasting Effects of Central Alpha-1-Adrenoreceptor Activation on Stress-Responsive and Stress-Nonresponsive Subpopulations of Corticotropin-Releasing Hormone Neurosecretory Cells in the Rat

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