Secondary to excessive melatonin synthesis, the consumption of tryptophan from outside the blood-brain barrier and melatonin over-signaling in the pars tuberalis may be central to the pathophysiology of winter depression

Pereira, José Carlos; Hallinan, Márcia Pradella; Alves, Rosana Cardoso

doi:10.1016/j.mehy.2016.11.020

Cited by 18 publications

(10 citation statements)

References 63 publications

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“…SAD is commonly characterized as reoccurring fall/winter depression with spontaneous remissions occurring in the spring/summer [ 8 ]. It has been proposed that winter depression in SAD is caused by an expansion and/or delay in the offset of melatonin secretion, driven by photoperiodic changes in SCN activity (as reviewed in [ 241 , 242 ]). From rodent work, it is known that during short winter-like days the peak of SCN neuronal activity is compressed, whereas during long summer-like days the peak of SCN neuronal activity is expanded [ 243 ].…”

Section: Light Cycle Manipulations and The Scnmentioning

confidence: 99%

Circadian Rhythm Disturbances in Mood Disorders: Insights into the Role of the Suprachiasmatic Nucleus

2017

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Circadian rhythm disturbances are a common symptom among individuals with mood disorders. The suprachiasmatic nucleus (SCN), in the ventral part of the anterior hypothalamus, orchestrates physiological and behavioral circadian rhythms. The SCN consists of self-sustaining oscillators and receives photic and nonphotic cues, which entrain the SCN to the external environment. In turn, through synaptic and hormonal mechanisms, the SCN can drive and synchronize circadian rhythms in extra-SCN brain regions and peripheral tissues. Thus, genetic or environmental perturbations of SCN rhythms could disrupt brain regions more closely related to mood regulation and cause mood disturbances. Here, we review clinical and preclinical studies that provide evidence both for and against a causal role for the SCN in mood disorders.

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Section: Light Cycle Manipulations and The Scnmentioning

confidence: 99%

Circadian Rhythm Disturbances in Mood Disorders: Insights into the Role of the Suprachiasmatic Nucleus

2017

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“…However, this pharmacotherapeutic evidence was non-specific to serotonin, and ironically, notwithstanding the risk of oversimplifying neural bases to complex disorders, the best evidence for a major role for CNS 5-HT in control of affect has come from studies that manipulate TRP entry to the brain ( 26 ) . Furthermore, whilst recent studies combining neuroimaging with administration of selective serotonin reuptake inhibitors have also strengthened the evidence for a role for central 5-HT in depression ( 27 ) , other evidence is emerging for the importance of peripheral metabolic pathways for TRP, including roles in inflammatory processes and melatonin synthesis, underlying major depression, seasonal affective disorder and bipolar disorder ( 1 , 11 , 12 , 28 ) .…”

Section: Serotonin and Behaviourmentioning

confidence: 99%

Tryptophan supplementation and serotonin function: genetic variations in behavioural effects

Gibson

2018

Proc. Nutr. Soc.

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The neurotransmitter serotonin has a role in affective disorders such as depression and anxiety, as well as sleep, cognitive function and appetite. This review examines the evidence that serotonin-related genotypes may moderate the behavioural effects of supplementation with the serotonin precursor amino acid l-tryptophan (TRP), on which synthesis of serotonin (or 5-hydroxytryptamine; 5-HT) depends. However, 95 % of serotonin is synthesised and used in the periphery, and TRP is also metabolised via non-5-HT routes such as the kynurenine pathway. Moreover, understanding of genotypes involved in regulation of serotonin raises questions over the generalisability of TRP effects on behaviour across individuals with varied serotonergic genotypes. To date, only differences between variants of the 5-HT transporter-linked promoter region (5-HTTLPR) have been investigated in relation to behavioural effects of TRP supplementation. Effects of 5-HTTLPR genotypes are usually compared between the alleles that are either high (L/L') or low (S/S') expressing of mRNA for the 5-HT transporter receptor. Yet, another key genetic variable is sex: in women, the S/S' genotype predicts sensitivity to improved mood and reduced cortisol by TRP supplementation, during stressful challenges, whereas the L/L' genotype protects against stress-induced mood deterioration. In men, the L/L' genotype may confer risk of stress-induced increases in negative affect; there are insufficient data to assess effects on male S/S' genotypes. However, better-powered studies to detect sex by genotype by stress by TRP interactions, as well as consideration of more genotypes, are needed before strong conclusions and recommendations for behavioural effects of TRP treatment can be reached.

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“…Thus, a decreased melatonin level may also reveal serotonin function disorders, as serotonin is a precursor of melatonin (Fig. 1) [22, 23]. …”

Section: Melatonin Synthesismentioning

confidence: 99%

“…Its reduced supply and difficult passage through the blood-brain barrier to serotoninergic neurons can lead to a decrease in serotonin synthesis. Therefore, a diet rich in both tryptophan and exogenous melatonin may have a beneficial effect on wellbeing [23]. …”

Section: Diets With Tryptophan and Melatoninmentioning

confidence: 99%

Pathophysiology of Depression: Molecular Regulation of Melatonin Homeostasis – Current Status

Dmitrzak‐Węglarz

Reszka

2017

Neuropsychobiology

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Circadian rhythm alterations resulting in disturbed sleep and disturbed melatonin secretion are flagship features of depression. Melatonin, known as a hormone of darkness, is secreted by the pineal gland located near to the center of the brain between the two hemispheres. Melatonin has an antidepressant effect by maintaining the body’s circadian rhythm, by regulating the pattern of expression of the clock genes in the suprachiasmatic nucleus (SCN) and modifying the key genes of serotoninergic neurotransmission that are linked with a depressive mood. Melatonin is produced via the metabolism of serotonin in two steps which are catalyzed by serotonin N-acetyltransferase (SNAT) and acetylserotonin-O-methyltransferase (ASMT). Serotonin, SNAT, and ASMT are key melatonin level regulation factors. Melatonin acts mainly on the MT₁ and MT₂ receptors, which are present in the SCN, to regulate physiological and neuroendocrine functions including circadian entrainment, referred to as a chronobiotic effect. Although melatonin has been known about and refereed to for almost 50 years, the relationship between melatonin and depression is still not clear. In this review, we summarize current knowledge about the genetic and epigenetic regulation of enzymes involved in melatonin synthesis and metabolism as potential features of depression pathophysiology and treatment. Confirmation that melatonin metabolism in peripheral blood partially reflects a disorder in the brain could be a breakthrough in the standardization of measurements of melatonin level for the development of treatment standards, finding new therapeutic targets, and elaborating simple noninvasive clinical tests.

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Secondary to excessive melatonin synthesis, the consumption of tryptophan from outside the blood-brain barrier and melatonin over-signaling in the pars tuberalis may be central to the pathophysiology of winter depression

Cited by 18 publications

References 63 publications

Circadian Rhythm Disturbances in Mood Disorders: Insights into the Role of the Suprachiasmatic Nucleus

Circadian Rhythm Disturbances in Mood Disorders: Insights into the Role of the Suprachiasmatic Nucleus

Tryptophan supplementation and serotonin function: genetic variations in behavioural effects

Pathophysiology of Depression: Molecular Regulation of Melatonin Homeostasis – Current Status

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