How important is stimulation of α‐adrenoceptors for melatonin production in rat pineal glands?

Tobin, Vicky; McCance, I.; Coleman, Harold A.; Parkington, Helena C.

doi:10.1034/j.1600-079x.2002.01842.x

Cited by 7 publications

(7 citation statements)

References 22 publications

(41 reference statements)

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“…It is important to point out that neural release of noradrenaline only activates β‐adrenoceptors because its effect is fully blocked by propranolol, a β‐adrenoreceptors competitive antagonist (38). In addition, activation of α‐adrenoceptors enhances the production of melatonin in cultured but not in freshly‐isolated rat pineal glands (39, 40). In such a context, the effect of corticosterone in vivo may be due to the interaction between high levels of glucocorticoids and β‐adrenergic stimulation.…”

Section: Discussionmentioning

confidence: 99%

Local Corticosterone Infusion Enhances Nocturnal Pineal Melatonin Production In Vivo

Fernandes

Bothorel

Clesse

et al. 2009

J Neuroendocrinology

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Melatonin, an important marker of the endogenous rhythmicity in mammals, also plays a role in the body defence against pathogens and injuries. In vitro experiments have shown that either pro- or anti-inflammatory agents, acting directly in the organ, are able to change noradrenaline-induced pineal indoleamine production. Whereas corticosterone potentiates melatonin production, incubation of the gland with tumour necrosis factor-alpha decreases pineal hormonal production. In the present study, we show that nocturnal melatonin production measured by intra-pineal microdialysis is enhanced in pineals perfused with corticosterone at concentrations similar to those measured in inflamed animals. In vitro experiments suggest that this enhancement may be due to an increase in the activity of the two enzymes that convert serotonin to N-acetylserotonin (NAS) and NAS to melatonin. The present results support the hypothesis that the pineal gland is a sensor of inflammation mediators and that it plays a central role in the control of the inflammatory response.

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Section: Discussionmentioning

confidence: 99%

Local Corticosterone Infusion Enhances Nocturnal Pineal Melatonin Production In Vivo

Fernandes

Bothorel

Clesse

et al. 2009

J Neuroendocrinology

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“…The hormonal production induced by the electrical field stimulation of the sympathetic nerve terminals of the pineal gland is completely abolished by β-adrenergic blockers [33], with α 1 -adrenoceptor activation seeming to have a relatively small effect on pineal melatonin production in vivo [37,38,39]. Defense responses increase circulating [35] and cervical superior ganglia (which innervates the pineal gland) release of catecholamines [34], leading to maximal adrenergic (β+α 1 ) pineal stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…Although the potentiation of pineal hormonal production by cultured glands following α 1 -adrenergic activation is well demonstrated [36], the involvement of this receptor in the modulation of nocturnal melatonin production in vivo remains controversial. Some reports have detected only a small contribution of α 1 -adrenoceptors [37], whereas others observed no effect [38] or even suggested an antagonistic interaction between α 1 - and β-adrenoceptors [39] with regard to the nocturnal melatonin surge. …”

Section: Introductionmentioning

confidence: 99%

Dual Effect of Catecholamines and Corticosterone Crosstalk on Pineal Gland Melatonin Synthesis

et al. 2016

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Background/Aim: The nocturnal production of melatonin by the pineal gland is triggered by sympathetic activation of adrenoceptors and may be modulated by immunological signals. The effect of glucocorticoids on nocturnal melatonin synthesis is controversial; both stimulatory and inhibitory effects have been reported. During pathophysiological processes, an increased sympathetic tonus could result in different patterns of adrenoceptor activation in the pineal gland. Therefore, in this investigation, we evaluated whether the pattern of adrenergic stimulation of the pineal gland drives the direction of the glucocorticoid effect on melatonin production. Methods: The corticosterone effect on the pineal hormonal production induced by β-adrenoceptor or β+α₁-adrenoceptor activation was evaluated in cultured glands. We also investigated whether the in vivo lipopolysaccharide (LPS)-induced inhibition of melatonin is dependent on the interaction of glucocorticoids and the α₁-adrenoceptor in adrenalectomized animals and on the in vivo blockade of glucocorticoid receptors (GRs) or the α₁-adrenoceptor. Results: Corticosterone potentiated β-adrenoceptor-induced pineal melatonin synthesis, whilst corticosterone-dependent inhibition was observed when melatonin production was induced by β+α₁-adrenoceptors agonists. The inhibitory effect of corticosterone is mediated by GR, as it was abolished in the presence of a GR antagonist. Moreover, LPS-induced reduction in melatonin nocturnal plasma content was reversed by adrenalectomy and by antagonizing GR or α₁-adrenoceptors. Conclusions: The dual effect of corticosterone on pineal melatonin synthesis is determined by the activation pattern of adrenoceptors (β or β+α₁) in the gland during GR activation, suggesting that increased activation of the sympathetic system and the hypothalamic-pituitary-adrenal axis are necessary for the control of melatonin production during defense responses.

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“…ß 1 -Adrenoceptor activation is an essential step and promotes, in rat pinealocytes, a cyclic AMP-dependent increase in NAT transcription; while · 1 -adrenoceptor activation has no effect alone, it potentiates ß-adrenergic response through an increase in intracellular calcium concentration ([Ca 2+ ] i ) [5]. It is interesting to note that, in vivo, the stimulation of ·-adrenoceptors does not potentiate cyclic AMP activation of N-acetyltransferase in rat pineal glands [6]. On the other hand, ATP, which also potentiates ß-adrenoceptorinduced N-acetylserotonin production [4], is released from the pineal nerve terminal together with noradrenaline [2].…”

Section: Introductionmentioning

confidence: 99%

P2Y<sub>1</sub> Receptor Activation Enhances the Rate of Rat Pinealocyte-Induced Extracellular Acidification via a Calcium-Dependent Mechanism

et al. 2003

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Pineal gland G-protein coupled P2Y₁ receptors potentiate noradrenaline-induced N′-acetylserotonin production, a long term response which occurs after 5 h incubation. In the current study we show that a short-term effect of stimulation of P2Y₁ receptors is the increase in extracellular acidification rate (ECAR), which is mediated by an increase in intracellular calcium concentration ([Ca²⁺]_i). The pD₂ values for ATP (3.06 ± 0.12)-induced ECAR increase was significantly smaller (p < 0.01) than that for ADP (3.64 ± 0.18), 2MeSATP (3.56 ± 0.02) and 2MeSADP (3.65 ± 0.13). The selective P2Y₁ receptor antagonists A3′P-5′P and A3′P-5′PS inhibited the increase in ECAR-induced by ADP. Clamping [Ca²⁺]_i with BAPTA (30 and 50 µmol/l) led to inhibition of ADP-induced increase in ECAR. Agonist and antagonist data indicate P2Y₁ activation leads to a [Ca²⁺]_i-dependent acidification of the extracellular medium.

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How important is stimulation of α‐adrenoceptors for melatonin production in rat pineal glands?

Cited by 7 publications

References 22 publications

Local Corticosterone Infusion Enhances Nocturnal Pineal Melatonin Production In Vivo

Local Corticosterone Infusion Enhances Nocturnal Pineal Melatonin Production In Vivo

Dual Effect of Catecholamines and Corticosterone Crosstalk on Pineal Gland Melatonin Synthesis

P2Y<sub>1</sub> Receptor Activation Enhances the Rate of Rat Pinealocyte-Induced Extracellular Acidification via a Calcium-Dependent Mechanism

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