Catecholamine effects upon rat hypothalamic corticotropin-releasing hormone secretion in vitro.
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To further our understanding of the functional role of catecholaminergic systems in regulating hypothalamic corticotropin-releasing hormone (CRH) secretion, we assessed the direct effects of a multiplicity of catecholamine agonists and antagonists on hypothalamic CRH secretion. To accomplish this, we used an in vitro rat hypothalamic organ culture system in which CRH secretion from single explants was evaluated by a specific RIA (IR-rCRH). Norepinephrine (NE) stimulated IR-rCRH secretion dose dependently, with peak effects in the nanomolar range. The effect of NE was antagonized by the mixed alpha antagonist phentolamine, the alpha 1 antagonist prazosin, and the alpha 2 antagonist yohimbine, but not by the beta blocker, L-propanolol. Compatible with these data were the findings that the alpha 1 agonist phenylephrine and the alpha 2 agonist clonidine both stimulated IR-rCRH secretion in a dose-dependent fashion. On the other hand, whereas the beta agonist, isoproterenol, caused a weak, non-dose-dependent increase in IR-rCRH secretion, this effect could not be antagonized by L-propanolol. Despite pretreatment with serotonin and acetylcholine antagonists, the effect of NE upon IR-rCRH secretion was undiminished, suggesting that NE-induced CRH secretion is not mediated by either neurotransmitter. On the other hand, pretreatment with gamma-aminobutyric acid (GABA) attenuated NE-induced IR-rCRH secretion. Whereas epinephrine (E) stimulated IR-rCRH secretion, this occurred only at higher concentrations, and was antagonized by phentolamine, but not by L-propanolol. Dopamine (DA) had a weak stimulatory effect that could be antagonized by the DA1 receptor antagonist, SCH 23390, but not by phentolamine. We conclude that NE and E stimulate hypothalamic IR-rCRH secretion via alpha 1 and alpha 2 receptors. The effect of NE upon IR-rCRH secretion is not apparently mediated by serotonergic or cholinergic interneurons, but is modulated by the inhibitory neurotransmitter, GABA. These data support the idea that the central catecholaminergic systems are excitatory rather than inhibitory upon CRH secretion when acting directly at the hypothalamic level.
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Neurotransmitters regulate peripheral cytokines through cortisol levels; acetylcholine, dopamine, and noradrenaline promote CRH secretion in the hypothalamus, and serotonin inhibits CRH secretion in the hypothalamus and ACTH in the pituitary.
“Neurotransmitters regulate peripheral cytokines through cortisol levels. For example, acetylcholine (Ach), dopamine (DA), and noradrenaline (NA) promote the secretion of corticotropin-releasing hormone (CRH) in the hypothalamus, and serotonin (5-HT) inhibits the secretion of CRH in the hypothalamus and adrenocorticotropic hormone (ACTH) in the pituitary[7].”
From Neuroinflammation and cytokine abnormality in major depression: cause or consequence in that illness? (2016) · cites this paper as [7]
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“CRH is positively regulated by serotonergic [93–95], cholinergic [96,97], and catecholaminergic [98] systems.”
BackgroundCentral effects of CRF on metabolism and energy balance
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Metyrapone as Additive Treatment in Major Depression: A Double-blind and Placebo-Controlled Trial
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“The effects of CRH are modulated by neuropeptides(7-9) and monoaminergic transmitters.(10,11) The exaggerated HPA function in depression appears to be also the result of an impaired glucocorticoid receptor (GR)(12,13) and mineralocorticoid receptor (MR)(14,15) feedback control.”
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“According to our data, NEis a potent stimulatory neurotransmitter for the central component of the HPAaxis (44), rather than inhibitory as previously suggested (51).”
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“Furthermore, the administration of CRF onto LC neurons increases the LC firing rate (Dunn and Berridge, 1990; Jedema and Grace, 2004), while norepinephrine is a potent stimulus for the release of CRF (Calogero et al., 1988; Cunningham et al., 1990).”
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Self-citationMolecular aspects of depression: A review from neurobiology to treatment
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“In support of a stimulatory effect of the α2-adrenoceptor on the HPA axis, clonidine has been reported to enhance CRH secretion from organotypic hypothalamic cultures (Calogero et al., 1988), and intracerebroventricular (Szafarczyk et al.”
BackgroundInfluentialHypothalamic-pituitary-adrenal axis dysregulation among diabetic outpatients
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“Norepinephrine is a potent stimulus of hypothalamic CRH release”
Kamilaris, T. C., Johnson, E. O., Calogero, A. E., Kalogeras, K. T., Bernardini, R., Chrousos, G. P., & Gold, P. W. (1992) · Endocrinology · doi:10.1210/endo.130.4.1312423 · Cited by 92 · see citing works
Self-citationAdrenergic control of the secretion of anterior pituitary hormones
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Cocaine stimulates rat hypothalamic corticotropin-releasing hormone secretion in vitro
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“…stimulation of a1 and a2 adrenoreceptors (AR) plays major roles in modulating limbic–hypothalamic–pituitary– adrenal axis responses during stress (Calogero et al, 1988; Online publication: 17 November 2005 at http://www.acnp.org/ citations/Npp111705050624/default.pdf Received 12 October 2005;…”
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“Erica Crespi provided valuable comments on the manuscript.”
BackgroundStress, antidepressant drugs, and the locus coeruleus
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Diabetic neuropathy is associated with increased activity of the hypothalamic-pituitary-adrenal axis
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Neuropeptide-Y stimulates CRF-41 release from rat hypothalami in vitro
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“In vitro results are, again, controversial, suggesting an involvement of at-, a2- [93], or f-adrenoceptors [92].”
BackgroundThe stress response and autoimmunoregulation
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Neuroendocrine Immunoregulation in Multiple Sclerosis
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“The secretion of CRH is upregulated by serotonergic [6], cholinergic [7], and catecholaminergic systems [8].”
BackgroundNeurotransmitter regulation of the hypothalamic corticotropin-releasing hormone neuron
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“Animal studies suggest that activation of α1-adrenoceptors stimulates the secretion of CRH and vasopressin (Hiwatari and Johnston, 1985; Plotsky, 1987; Szafarczyk et al., 1987; Calogero et al., 1988; Hillhouse and Milton, 1989) whereas α2-adrenergic mechanisms play rather a modulatory inhibitory role with regard to hy…”
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“, 2000) and stimulates CRH release ex vivo (Fehm et al., 1980; Calogero et al., 1988) and in vivo, as inferred from rises in circulating ACTH (Itoi et al.”
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Self-citationStress and the CRH System, Norepinephrine, Depression, and Type 2 Diabetes
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“…the increase in central NE secretion, triggered by the limbic response to CRH [44]; in turn, NE stimulates the secretion of adrenal cortisol [41,45] and, through positive feedback, also the hypothalamic and limbic secretion of CRH, supporting the central hyperactivation of the HPA system [46,47].”
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“CRH and noradrenergic neurons of the central stress system innervate and stimulate each other by positive feedback, such that activation of one system leads to activation of the other ( 30 ).”
BackgroundDiazepam‐binding inhibitor and corticotropin‐releasing hormone in cerebrospinal fluid
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“In vivo studies with rat hypothalamic nuclei have shown that both NE and acetylcholine stimulate the secretion of CRH (22, 23).”
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Investigating the Molecular Basis of Major Depressive Disorder Etiology
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- Authors
- Calogero, A. E., Gallucci, W. T., Chrousos, G. P., & Gold, P. W.
- Affiliations
- National Institutes of Health (US)
- National Institute of Mental Health (US)
- ORCID
- Calogero, A E
- Venue
- Journal of Clinical Investigation
- Published
- 1988-09-01
- Volume
- 82
- Issue
- 3
- Pages
- 839-846
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC303591
- OpenAlex
- W2099891752
- Cited by
- 188
- References
- 66
- Citations by year
- 2024: 3 · 2023: 2 · 2022: 1 · 2021: 4 · 2020: 2 · 2019: 3 · 2018: 2 · 2016: 1 · 2015: 3 · 2014: 3 · 2013: 4 · 2012: 3
- FWCI
- 8.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- catecholamines, corticotropin-releasing factor, hypothalamus, norepinephrine, epinephrine, dopamine, alpha1-adrenoceptors, alpha2-adrenoceptors, GABA, phentolamine, prazosin, yohimbine, isoproterenol, serotonin, acetylcholine, hypothalamic-pituitary-adrenal axis
- MeSH terms
- Adrenergic alpha-Agonists, Adrenergic alpha-Antagonists, Adrenergic beta-Agonists, Adrenergic beta-Antagonists, Animals, Catecholamines, Corticotropin-Releasing Hormone, Dopamine, Epinephrine, Hypothalamus, Male, Organ Culture Techniques, Rats, Inbred Strains, Rats
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