Kinetic changes of melatonin release in rat pineal perifusions at different circadian stages. Effects of corticosteroids

Zhao, Ziyan; Touitou, Yvan

doi:10.1530/acta.0.1290081

Cited by 33 publications

(20 citation statements)

References 16 publications

(32 reference statements)

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“…However, previous literature data show controversial results regarding this crosstalk, indicating both stimulatory and inhibitory effects of glucocorticoids on pineal melatonin synthesis [9,21,22,23,24,25,26,27,28,29]. The present study shows that the pattern of adrenergic activation in the pineal gland regulates the direction of the corticosterone effect on melatonin synthesis (fig.…”

Section: Discussionmentioning

confidence: 42%

“…Corticosterone may either potentiate or inhibit melatonin production when cultured pineal glands are stimulated by a low [9,21] or a high [22] concentration of noradrenaline, respectively. Similarly, in vivo data show that perfusion of a high corticosterone concentration [23], or stress-induced plasma corticosterone elevation [24,25], inhibits pineal melatonin synthesis. This contrasts to transpineal infusion of a high corticosterone concentration [26], mild restraint stress in rats [27] or thermic stress in goats [28], which potentiate pineal melatonin production.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 42%

Section: Introductionmentioning

confidence: 99%

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

et al. 2016

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“…The remaining pineals were kept in oxygenated Krebs-Ringer solution in an iced water bath until their transfer to the perifusion chambers. The perifusion protocol has been described previously (18). Briefly, the perifusion system consisted of a plastic column closed with two pistons, a thermostatic bath which maintained the temperature at 37 Ϯ 0.5 Њ C, and a peristaltic pump.…”

Section: Methodsmentioning

confidence: 99%

Increased delta aminolevulinic acid and decreased pineal melatonin production. A common event in acute porphyria studies in the rat.

Puy¹,

Deybach²,

Bogdan³

et al. 1996

J. Clin. Invest.

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Tryptophan (TRP) is the precursor of melatonin, the primary secretory product of the pineal gland. Hepatic heme deficiency decreases the activity of liver tryptophan pyrrolase, leading to increased plasma TRP and serotonin. As a paradox, patients with attacks of acute intermittent porphyria (AIP), exhibit low nocturnal plasma melatonin levels. This study using a rat experimental model was designed to produce a pattern of TRP and melatonin production similar to that in AIP patients.Pineal melatonin production was measured in response to: ( a ) a heme synthesis inhibitor, succinylacetone, ( b ) a heme precursor, ␦ -aminolevulinic acid (Ala), ( c ) a structural analogue of Ala, ␥ -aminobutyric acid. Studies were performed in intact rats, perifused pineal glands, and pinealocyte cultures. Ala, succinylacetone, and ␥ -aminobutyric acid significantly decreased plasma melatonin levels independently of blood TRP concentration. In the pineal gland, the key enzyme activities of melatonin synthesis were unchanged for hydroxyindole-O-methyltransferase and decreased for N -acetyltransferase.Our results strongly suggest that Ala overproduced by the liver acts by mimicking the effects of ␥ -aminobutyric acid on pineal melatonin production. These data could account for the low plasma melatonin in AIP. They also support the view that Ala acts as a toxic element in the pathophysiology of AIP. ( J. Clin. Invest. 1996. 97:104-110.) Key words: porphyria • melatonin • ␦ -aminolevulinic acid • tryptophan • ␥ -aminobutyric acid

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“…In human and rat, nighttime stress reduced M production while daytime stress increased M production (Monteleone et al, 1992). Pharmacological doses of GC, however, attenuated M production, whatever the circadian stage (Zhao and Touitou, 1993). Though inconsistent, the reported data suggest a functional, circadian modulated antagonism between M and GC.…”

Section: The Hormones and Neuropeptides Establish An Interactive Networkmentioning

confidence: 94%

A unifying hypothesis of Alzheimer's disease. I. Ageing sets the stage

Heininger

1999

Hum. Psychopharmacol. Clin. Exp.

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In a series of ®ve papers, evidence from neurobiology, endocrinology and immunology is integrated into a holistic, coherent hypothesis accommodating genetic, medical and environmental risk factors into a cascade of pathophysiological events that leads to the clinical manifestation of Alzheimer's disease (AD). The perturbation of the calcium-energy-oxidative stress triangle emerges as pathophysiological leitmotif of ageing and AD. Cellular Ca 2 homeostasis and energy metabolism are closely interdependent. Ca 2 ions regulate the activity of a variety of ratelimiting enzymes of the tricarboxylic acid cycle and respiratory chain. Under physiological circumstances, the supply of energy according to demand is regulated by Ca 2 cycling across mitochondrial membranes. In certain pathological conditions, Ca 2 uncouples electron transfer and oxidative phosphorylation and increases the mitochondrial production of oxygen radicals which in tandem with Ca 2 precipitate the breakdown of mitochondrial function and structure. As most important risk factor, ageing sets the stage for the development of AD. The delicate regulation of the neuroendocrine network which physiologically modulates the Ca 2 -energy-redox homeostasis, deteriorates in ageing, compromising the hormonal balance between neurotrophic/protective and neuroaggressive factors. Thus, levels and/or signal transduction pathways of neurotrophic-factors such as neuropeptide Y, neurotrophins, DHEA/ DHEAS, gonadal hormones, melatonin, insulin, insulin-like growth factors, somatostatin, thyroid hormones, and substance P decay, paralleled by the compromise of the hypothalmic-pituitary-adrenal (HPA)-axis feedback inhibition leading to a hyperresponsiveness to stress and a loss of diurnal rhythm of secretion of neuroaggressive glucocorticoids. Both add up to disrupt Ca 2 and energy homeostasis, put the nerve cells under metabolic and oxidative stress and lead to a compromise of neuronal excitability, signal transduction processes and neuronal plasticity. Subject to the same endocrinological dysregulation, the ageing immune system exhibits a primitive response pattern with impairment of speci®c cellular and activation of unspeci®c humoral and microglial immune responses. Thus, the ageing-related concerted perturbation of the homeostatic control in the neuroendocrinoimmunological network creates phenomena which in many aspects are qualitatively similar to changes in AD and lay the foundations for the development of the disease.

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Kinetic changes of melatonin release in rat pineal perifusions at different circadian stages. Effects of corticosteroids

Cited by 33 publications

References 16 publications

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

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

Increased delta aminolevulinic acid and decreased pineal melatonin production. A common event in acute porphyria studies in the rat.

A unifying hypothesis of Alzheimer's disease. I. Ageing sets the stage

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