Taste plays a fundamental role in an animal’s ability to detect nutrients and transmits key dietary information to the brain, which is crucial for its growth and survival. Providing alternative terrestrial ingredients early in feeding influences the growth of rainbow trout (RT, Oncorhynchus mykiss). Thus, the present study aimed to assess the influence, via long-term feeding (from the first feeding to 8 months), of alternative plant ingredients (V diet for vegetable diet v. C diet for a control diet) in RT on the mechanism of fat sensing at the gustatory level. After the feeding trial, we studied the pathways of the fat-sensing mechanism in tongue tissue and the integrated response in the brain. To this end, we analysed the expression pattern of free fatty acid receptors (ffar) 1 and 2, markers of calcium-signalling pathways (phospholipase Cβ, Orai, Stim or Serca), the serotonin level (a key neurotransmitter in taste buds) and the expression pattern of appetite-regulating neuropeptides in the hypothalamus (central area of appetite regulation). The results revealed that the V diet modified the expression pattern of ffar1 and paralogs of ffar2 genes in tongue tissue, along with differential regulation of calcium-signalling pathways and a defect in serotonin level and brain turnover, without influencing neuropeptide expression. This study is the first to support that changes in feeding behaviour of RT fed a V diet could be due to the difference in nutrient sensing and a decrease in hedonic sensation. We revealed that RT have similar fat-detection mechanisms as mammals.

Two X-linked microsatellites, (AC)n repeats at the monoamine oxidase (MAO) A locus and (TG)n repeats at the MAO-B locus, were typed by using a PCR-based procedure in 89 nuclear families consisting of mothers, fathers and female affected offspring with schizophrenia or mothers and male affected offspring. A haplotype-based haplotype relative risk (HHRR) approach was applied to detect allelic association of these two microsatellites with schizophrenia. In the families of male patients, a significant difference in frequency distribution was found between transmitted and non-transmitted (TG)n repeats (χ2 = 15.13, df = 6, P = 0.019), and Fisher's exact test showed that allelic frequency of the transmitted (TG)24 was significantly higher than that of the non-transmitted (TG)24 (Fisher's P = 0.003). However, no significant differences in frequency distribution between mother- or father-transmitted and non-transmitted (TG)n repeats were found in the families of female patients. No significant differences in frequency distribution were found between transmitted and non-transmitted (AC)n repeats in the families of either male patients or female patients. The present study suggests that the MAO-B gene may be associated with schizophrenia, and the underlying genetic mechanism of schizophrenia may differ between male and female schizophrenic individuals.

In summary, genetics, as well as foetal and early life environmental factors shape the size or capacity of our monoamine systems, of which the serotonergic one might play a leading role. Those constitutional properties then form the biological basis for personality traits, such as impulsiveness and “sensation seeking”, which interact with psychosocial settings and life events to form a pattern of reactivity to a current life event or psychosocial situation, shown as a high or low order of magnitude of gene-environment interaction. In the present paper emphasis is put on the role of genotypes of the serotonin transporter, of monoamine oxidases A and B, and of platelet monoamine oxidase B activity, which all have been shown to be of importance for behaviour and with obvious effects of interactions with environment. Under unfortunate circumstances constitutional properties might be strong enough to result in vulnerability for suicide, even with a modest influence of environment.

The present study investigated the effects of Porphyra yezoensis enzyme degradation extract (PYEDE) on the brain injuries and neurodegenerative diseases due to oxidative stress. We used in vitro antioxidant systems to verify the antioxidant potential of PYEDE. The results indicated that the PYEDE alleviated weight loss and organ atrophy, reduced the levels of lipid peroxidation and protein carbonylation and elevated reduced glutathione (GSH) content in the serum and brains of the d-galactose-induced ageing model mice. The PYEDE also renewed the glutathione peroxidase (GSH-Px), superoxide dismutase and total antioxidant capability activities, down-regulated the inducible nitric oxide synthase activity and nitric oxide levels, normalised the hippocampal neurons and modulated multiple neurotransmitter systems by inhibiting the activities of acetylcholinesterase and monoamine oxidase in the up-regulation of acetylcholine, dopamine and noradrenaline levels. Overall, the PYEDE is a promising supplement for the alleviation of oxidative stress and age-associated brain diseases.

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.

Despite the fact that monoamine oxidase inhibitors (MAOIs) can be highly effective therapeutic agents for depression and some anxiety disorders, they tend to be underutilized in clinical practice. This is due at least in part to the fact that there is a great deal of misinformation and mythology about their dietary and drug interactions. This article is intended to serve as a guide for clinicians who are not particularly familiar with MAO inhibitors; its aim is to help these clinicians competently integrate these agents into clinical practice when appropriate.

Objective: The blood platelet has been proposed as a model of central neurons and may therefore be used as a peripheral marker of psychiatric illness. One method of investigating serotonin function in panic disorder has relied on the use of the platelet as a model of serotonergic neurons. This article reviews the studies of platelet function in panic disorder.

Method: A literature search and review of relevant papers was undertaken.

Result: Studies examining platelet serotonin uptake and concentration in panic disorder patients have to date yielded conflicting results, with some investigators reporting increased serotonin uptake, others reduced uptake. Similarly studies of platelet 3H-imipramine binding have also yielded conflicting results. Two studies of platelet 3H-paroxetine binding have shown a reduction in the density of binding sites (Bmax) in patients with panic disorder. Platelet monoamine oxidase activity in anxiety disorders has been reported to be increased by some investigators but decreased by others. Methodological considerations may have been responsible for these differences. Finally, studies of α2 adrenoceptor density have also produced contrasting findings.

Conclusion: The findings of these studies indicate that platelet function is altered in panic disorder. Such changes may allow an insight into the biochemical aetiology of the illness. Further studies are required to delineate the role of serotonin and non-adrenaline in panic disorder.

A comparative study was carried out between a control group and different patient subgroups suffering from psychosonratic disorders: headache, insomnia and loss of consciousness due to neurocirculatory dystonia.

Different personality questionnaires (Minnesota Multiphasic Personality Inventory, Sensation Seeking Scale, Susceptibility to Punishment Scale), neurobioelectric parameters (Hjörth descriptors, alpha percentage, P100, N120 P200 of visual evoked responses) and platelet monoamine oxidase B (using phenylethylamine as substrate) were evaluated.

The results show a significant increase in anxiety indicators (at a psychometric and bioelectric level) in the headache and insomnia groups. MAO B activity was higher in patients, especially in the insomniac group; but no significant differences were found in any of the groups studied.