BackgroundTryptophan (TRP) is an essential amino acid, and it has been suggested that TRP intake at breakfast combined with daytime bright light exposure can increase nocturnal melatonin secretion. However, the mechanisms involved are not yet clear. The aim of this study was to examine the effect of TRP supplement intake at breakfast on nocturnal melatonin secretion under different daytime light intensities in humans.MethodTwelve subjects (aged 21.3 ± 3.0 years, mean ± standard deviation) participated in a random order in experimental sessions lasting 3 days under four conditions in a laboratory setting. The four conditions were TRP*Bright, Placebo*Bright, TRP*Dim, and Placebo*Dim. A TRP capsule (1000 mg) or a placebo starch capsule (1000 mg) were taken at breakfast. In addition, during the daytime (07:00–18:00), the subjects were asked to stay under different light intensities: >5000 lx (bright) or <50 lx (dim). Saliva samples were collected for measuring the concentration of melatonin. The time courses of melatonin concentration and dim light melatonin onset (DLMO) were compared among the four conditions using repeated measurements analysis of variance (ANOVA).ResultNocturnal melatonin concentrations in the bright light condition tended to be higher than in the dim light condition (main effect of light: p = .099). Moreover, in the bright light condition, the change in DLMO between baseline and after the intervention was significantly higher than that in the dim light condition (main effect of light: p <.001). However, the ANOVA results indicated no significant effect of TRP intake on melatonin secretion.ConclusionOur findings indicated that intake of 1000 mg of TRP at breakfast on 1 day did not change nocturnal melatonin secretion, even though TRP is the precursor of melatonin. In contrast, daytime bright light exposure increased nocturnal melatonin secretion and advanced the phase of melatonin onset. Therefore, TRP supplementation, unlike exposure to daytime bright light, does not acutely affect biological rhythm and sleep in humans.Trial registrationUMIN Clinical Trial Registry: UMIN000024121 Electronic supplementary materialThe online version of this article (doi:10.1186/s40101-017-0135-9) contains supplementary material, which is available to authorized users.

This contribution aims to integrate findings of our recently reported three brain imaging studies on young narcolepsy-cataplexy patients [1][2][3]. All brain images were acquired using 3.0 Tesla MRI. In our prior study of a voxel-based morphometry [1], narcoleptic patients showed gray matter (GM) deficits in the hypothalamus and fronto-limbic areas. Hypothalamic GM deficits correlated with severity of narcolepsy. In our diffusion tensor imaging study that assessed global white matter (WM) integrity [2], narcoleptic patients had decreased WM integrity especially in fronto-limbic areas, which were associated with sleepiness and attention deficit. Prefrontal metabolite concentration was measured in a proton magnetic resonance spectroscopy [3]. Narcoleptic patients had higher GABA levels in the medial prefrontal areas. This is potentially related to the compensation of nocturnal sleep disturbance. Hypothalamus seems to be a key structure in narcoleptic symptoms. However, both GM and WM abnormalities of fronto-limbic areas were also related to narcolepsy and its symptoms. Compensatory alteration of GABA was also found in the areas. Taken together, our reports suggest that fronto-limbic area, as well as hypothalamus, may be implicated in narcolepsy. References[1] Gray matter deficits in young adults with narcolepsy. Acta Neurol Scand 2009;119:61-7. [2] Decreased fractional anisotropy values in brains of young narcoleptic patients. 2009; presented in APSS. [3] Increased GABA levels in medial prefrontal cortex of young adults with narcolepsy.Two types of monoamine oxidase (MAO), type A (MAO-A) and type B (MAO-B), have been identified. Generally, MAO-A is highly expressed in noradrenergic/adrenergic neurons such as the locus coeruleus, whereas MAO-B is highly expressed in serotonergic and histaminergic neurons and distinct populations of glia such as tanicytes. On the other hand, it has been reported that non-catecholaminergic neurons also express MAOs in an adult rat brain. Extracellular serotonin (5-HT), norepinephrine / epinephrine (NE/E), and dopamine (DA) appear to be removed by a reuptake mechanism; subsequently, they are metabolized by intracellular MAO activity. In the hypothalamus, 5-HT and DBHpositive varicosities densely distribute around hypothalamic nucleus, likely MAO activity affecting the neuronal functions. In the present study, we investigated the distribution of MAOs and the anatomical relation to the neuropeptide-expressing neurons in the rat hypothalamus. We performed enzyme histochemistry for MAO-A or MAO-B, and use specific antibodies for MAO-A and MAO-B. In the result, we found moderate MAO-A enzyme activities in the distinct neuronal populations, and strong MAO-B activity in some glial cells including tanicytes. MAO-A-immunoreactivities (IR) were found in the varicosities of noradrenergic/adrenergic neurons and in the cell bodies of some neuropeptides-expressing neurons in the lateral hypothalamus. Especially, orexin neurons robustly express MAO-A, but not MAO-B. Objective:We have elucidated the p...