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The Pineal Gland and Melatonin
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Jerry Vriend, Nancy A.M. Alexiuk
Although the pinealocyte is the most numerous and most extensively studied cell type in the mammalian pineal, other cell types have been observed. Glial cells have been estimated to account for up to 12% of the total number of cells in the rat pineal.100 Immunocytochemical studies of glial cells in the rat pineal provide evidence that the glial cells are primarily astrocytes.101 Astrocyte-specific glial antigens, vimenten, glial fibrillary acid protein (GFAP) and S-100 were localized in the pineal gland of rats, hamsters, and gerbils.23,102 Glial processes were also found in the pineal stalk, where they are described as encircling neural and vascular elements of the stalk.103
Pineal Gland
Published in Paul V. Malven, Mammalian Neuroendocrinology, 2019
The primary secretory product of the pineal gland is melatonin and Figure 10-1 summarizes melatonin biosynthesis. Pinealocytes take up blood-borne tryptophan and convert it into 5-hydroxytryptophan using the enzyme tryptophan hydroxylase. The 5-hydroxytryptophan is then decarboxylated to yield the indolamine compound serotonin (also known as 5-hydroxytryptamine or 5-HT). Neither enzymatic conversion leading to the formation of serotonin is thought to be rate-limiting to biosynthesis of melatonin. However, the conversion of serotonin into N-acetylserotonin by the enzyme N-acetyltransferase (NAT) is a highly regulated and very rate-limiting reaction in melatonin synthesis. The final biosynthetic step involves the conversion of N-acetylserotonin to melatonin (also known as 5-methyoxy N-acetylserotonin) by the enzyme hydroxyindole-O-methyltransferase (abbreviated HIOMT). Most of the melatonin synthesized in pinealocytes is secreted into blood. A small portion is secreted into the cerebrospinal fluid (CSF) of the third ventricle, and some may be metabolized within the pinealocytes to biologically weaker compounds. Although the concentrations of melatonin in blood and in CSF are approximately equivalent, quantitative analysis of melatonin secretion by the sheep pineal gland revealed that far greater amounts were secreted into blood than into CSF, reflecting the much larger volume of blood compared to CSF (Rollag et al., 1978).
The Pineal Gland
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
Although some animals reportedly have but one type of pinealocyte,92 most species studied in this context exhibit two distinctive cell forms.67,71,72,75,76,78,93–95 In the rat and hamster there is a layer of cells with large nuclei around the periphery of the pineal, with interior cells having smaller nuclei — giving an appearance, which may be artifactual, of a cortex and medulla.62 Various researchers have called the two populations Pinealocyte Type I (those with larger nuclei and dispersed chromatin) and Pinealocyte Type II (those with smaller nuclei and tightly packed chromatin).71 Type I nuclei appear light, and Type II dark,—hence the designations “light” and “dark” pinealocytes.
The melatonin receptor 1B gene links circadian rhythms and type 2 diabetes mellitus: an evolutionary story
Published in Annals of Medicine, 2023
Hui Zhu, Zhi-jia Zhao, Hong-yi Liu, Jie Cai, Qin-kang Lu, Lin-dan Ji, Jin Xu
Synthesis of the pineal hormone melatonin is regulated by the SCN master clock and synchronized to the environmental light-dark cycle. Melatonin secretion generally occurs in darkness (at night) and peaks at 00:00 and 4:00 am. Importantly, nighttime melatonin production is blocked by light, especially blue light at wavelengths of 460–480 nm and intensities < 200 lux [43–45]. The biosynthetic precursor of melatonin is tryptophan, which is hydroxylated to 5-hydroxytryptophan and then decarboxylated to generate serotonin. Subsequently, serotonin is acetylated to N-acetylserotonin by arylalkylamine N-acetyltransferase (AANAT) and then converted to melatonin by acetylserotonin O-methyltransferase [16]. When the environmental photoperiodic information reaches intrinsic photosensitive retinal ganglion cells (ipRGCs), it is conveyed to the SCN by the retinal hypothalamic tract. Afterward, the signal is projected to the pineal gland through a neuronal signaling cascade that promotes or inhibits melatonin secretion in pinealocytes (Figure 1) [41,46,47].
Night work effects on salivary cytokines TNF, IL-1β and IL-6
Published in Chronobiology International, 2019
Érica Lui Reinhardt, Pedro Augusto Carlos Magno Fernandes, Regina P. Markus, Frida Marina Fischer
Our results of salivary TNF and IL-1β are in agreement with their findings about cytokines, but not those regarding salivary IL-6. However, Cuesta et al. (2016) detected the presence of significant plasma melatonin rhythms following three simulated night shifts, without any significant phase shift or change in amplitude. In the present study, in contrast, a melatonin rhythm was absent and there were significant changes in melatonin amplitude among night workers. Recently, it was suggested a close relationship between melatonin and the synthesis of IL-6 by monocytes (Song et al. 2018). In addition, melatonin, at concentrations compatible to nocturnal plasma concentration (pM to nM), inhibits the rolling and adhesion of leukocytes (Lotufo et al. 2001; Markus et al. 2018). During the mounting of an inflammatory response the nocturnal melatonin peak is reduced or even absent, as the activation of the nuclear factor kappa B (NFκB) pathway in pinealocytes blocks the synthesis of melatonin in rodents and humans (Markus et al. 2018). Thus, the whole circadian system, including clocks and pineal gland, is involved in regulating cytokine profile in shift workers.
Pharmacotherapy and nutritional supplements for seasonal affective disorders: a systematic review
Published in Expert Opinion on Pharmacotherapy, 2018
Olivia Cools, Kaat Hebbrecht, Violette Coppens, Laurence Roosens, Andy De Witte, Manuel Morrens, Hugo Neels, Bernard Sabbe
Two beta-blockers have been shown to have certain positive effects on mood symptomatology and are hypothesized to suppress the nocturnal secretion of melatonin; melatonin is released in response to stimulation of the β-adrenergic receptors on the pinealocytes [66,67]. Atenolol, a long-acting beta-blocker, was compared with placebo [66]. Both groups significantly improved, but no significant differences were observed between them [66]. Schlager et al. [67] proposed that the failure of atenolol was due to its long-acting properties and hypothesized that a short-acting beta-blocker given before sunrise would be more beneficial [67]. Propranolol was investigated in a two-phase design with an introductory, open-label phase followed by a DB-RCT [67]. After the open-label phase (n = 33), depressive scores significantly decreased, with 24 out of 33 subjects being in remission. Only 12 subjects enrolled in the subsequent RCT. In the second phase, all subjects regained symptoms, although the severity of depressive symptomatology was significantly higher in the placebo group [67].