Melatonin formation in mammals: In vivo perspectives

Chattoraj, Asamanja; Liu, Tiecheng; Zhang, Liang Samantha; Huang, Zheping; Borjigin, Jimo

doi:10.1007/s11154-009-9125-5

Cited by 89 publications

(82 citation statements)

References 35 publications

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“…Dentro de los pinealicitos, los receptores activan la enzima adenilciclasa y posteriormente esta enzima activa el sistema AMPc, el cual se traduce en la síntesis de las enzimas N-acetil transferasa (NAT), enzima limitante de la velocidad de la biosíntesis de la melatonina, e hidroxindol-metiltransferasa (HIOMT). La NAT es la encargada de la N-acetilación y la HIOMT de la Ometilación de la serotonina, y la producción final de melatonina (Chattoraj, Liu, Zhang, Huang, & Borjigin, 2009;Goldman, 2001;B. Malpaux, Migaud, Tricoire, & Chemineau, 2001).…”

Section: Influencia De La Melatonina Sobre La Fisiología Y La Conductunclassified

Influencia de la Melatonina sobre la fisiología y la conducta de ungulados

Correa

Riveros

2017

Rev. Investig. Altoandin. - RIA -

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Section: Influencia De La Melatonina Sobre La Fisiología Y La Conductunclassified

Influencia de la Melatonina sobre la fisiología y la conducta de ungulados

Correa

Riveros

2017

Rev. Investig. Altoandin. - RIA -

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“…Both substances co-exist in the sympathetic nerve fibers, but NPY also occurs in a small population of non-sympathetic fibers, probably of the central origin , Zhang et al 1991, Møller et al, 1996, Møller 1999. Unquestionably, NE is the essential factor stimulating the secretory activity of pinealocytes in all mammals, however, the mechanisms of adrenergic regulation of melatonin synthesis exhibit strong species heterogeneity (Coon et al 1995, Schomerus 2000, Stehle et al 2001, Simonneaux and Ribelayga 2003, Lewczuk et al 2005, Chattoraj et al 2009). In contrast to NE, the role of NPY in the pineal gland physiology is poorly recognized, since the obtained experimental data are not univocal (Vacas et al 1987, Olcese 1991, Harada et al 1992, Simonneaux et al 1994a,b, Ribelayga et al 1998.…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y as a presynaptic modulator of norepinephrine release from the sympathetic nerve fibers in the pig pineal gland

Ziółkowska¹,

Lewczuk²,

Przybylska‐Gornowicz³

2015

Polish Journal of Veterinary Sciences

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Norepinephrine (NE) released from the sympathetic nerve endings is the main neurotransmitter controlling melatonin synthesis in the mammalian pineal gland. Although neuropeptide Y (NPY) co-exists with NE in the pineal sympathetic nerve fibers it also occurs in a population of non-adrenergic nerve fibers located in this gland. The role of NPY in pineal physiology is still enigmatic. The present study characterizes the effect of NPY on the depolarization-evoked 3 H-NE release from the pig pineal explants.The explants of the pig pineal gland were loaded with 3 H-NE in the presence of pargyline and superfused with Tyrode medium. They were exposed twice to the modified Tyrode medium containing 60 mM of K + to evoke the 3 H-NE release via depolarization. NPY, specific agonists of Y 1 -and Y 2 -receptors and pharmacologically active ligands of α 2 -adrenoceptors were added to the medium before and during the second depolarization. The radioactivity was measured in medium fractions collected every 2 minutes during the superfusion. NPY (0.1 -10 μM) significantly decreased the depolarization-induced 3 H-NE release. Similar effect was observed after the treatment with Y 2 -agonist: NPY 13-36 , but not with Y 1 -agonist: [Leu 31 ,Pro 34 ]-NPY. The tritium overflow was lower in the explants exposed to the 5 μM NPY and 1 μM rauwolscine than to rauwolscine only. The effects of 5 μM NPY and 0.05 μM UK 14,304 on the depolarization-evoked 3 H-NE release were additive.The results show that NPY is involved in the regulation of NE release from the sympathetic terminals in the pig pineal gland, inhibiting this process via Y 2 -receptors.

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“…The levels of NAS, synthesized by AANAT, can constrain the rate of melatonin synthesis from NAS during light parts of daily cycles (when NAS levels are low) but appear not to be the rate-limiting step during dark parts of these cycles, when both AANAT and NAS levels are high (21). In rodents such as rats, the activity of AANAT starts to increase 3-4 h after the onset of darkness and begins to decrease before the onset of light in the morning (21,31). Hence the importance of regulating the expression and the enzymatic activity of AANAT, because these parameters determine the levels of both NAS and melatonin.…”

mentioning

confidence: 99%

Degradation of Serotonin N-Acetyltransferase, a Circadian Regulator, by the N-end Rule Pathway

Wadas

Borjigin

Huang

et al. 2016

Journal of Biological Chemistry

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Serotonin N-acetyltransferase (AANAT) converts serotonin to N-acetylserotonin (NAS), a distinct biological regulator and the immediate precursor of melatonin, a circulating hormone that influences circadian processes, including sleep. N-terminal sequences of AANAT enzymes vary among vertebrates. Mechanisms that regulate the levels of AANAT are incompletely understood. Previous findings were consistent with the possibility that AANAT may be controlled through its degradation by the N-end rule pathway. By expressing the rat and human AANATs and their mutants not only in mammalian cells but also in the yeast Saccharomyces cerevisiae, and by taking advantage of yeast genetics, we show here that two "complementary" forms of rat AANAT are targeted for degradation by two "complementary" branches of the N-end rule pathway. Specifically, the N ␣ -terminally acetylated (Nt-acetylated) Ac-AANAT is destroyed through the recognition of its Nt-acetylated N-terminal Met residue by the Ac/N-end rule pathway, whereas the nonNt-acetylated AANAT is targeted by the Arg/N-end rule pathway, which recognizes the unacetylated N-terminal Met-Leu sequence of rat AANAT. We also show, by constructing lysineto-arginine mutants of rat AANAT, that its degradation is mediated by polyubiquitylation of its Lys residue(s). Human AANAT, whose N-terminal sequence differs from that of rodent AANATs, is longer-lived than its rat counterpart and appears to be refractory to degradation by the N-end rule pathway. Together, these and related results indicate both a major involvement of the N-end rule pathway in the control of rodent AANATs and substantial differences in the regulation of rodent and human AANATs that stem from differences in their N-terminal sequences.Arylalkylamine N-acetyltransferase (AANAT) 2 converts the neurotransmitter serotonin to N-acetylserotonin (NAS)(1-11). Regulatory functions of NAS include its activity as an agonist of TrkB, the receptor for the brain-derived neurotrophic factor (12)(13)(14). NAS is the immediate precursor of melatonin, a circulating hormone that regulates sleep and other circadian processes in vertebrates. Melatonin is also present in invertebrates, including insects, as well as in animals that lack recognizable neurons (1, 15-21). The functions of melatonin in mammals include the modulation of circadian rhythms in response to light-dark cycles. Melatonin also contributes to the control of seasonal physiology (20). These mechanisms are a part of a broader range of processes that involve distinct biological oscillators in all organisms (22-24). In the course of daily light-dark cycles, the activity of AANAT and the level of the ϳ23-kDa AANAT protein in the brain's pineal gland are high during nocturnal periods and rapidly decrease following exposure to light (1,20,25).In mammals, changes of AANAT levels in the brain's pineal gland are controlled by the circadian oscillator in the suprachiasmatic nucleus of the hypothalamus. At night, axons of rodent superior cervical ganglion neurons release norepinephrine i...

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Melatonin formation in mammals: In vivo perspectives

Cited by 89 publications

References 35 publications

Influencia de la Melatonina sobre la fisiología y la conducta de ungulados

Influencia de la Melatonina sobre la fisiología y la conducta de ungulados

Neuropeptide Y as a presynaptic modulator of norepinephrine release from the sympathetic nerve fibers in the pig pineal gland

Degradation of Serotonin N-Acetyltransferase, a Circadian Regulator, by the N-end Rule Pathway

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