# Tryptophan and Membrane Mobility as Conditioners and Brokers of Gut-Brain Axis in Depression
###### Abstract  
The aim of this brief narrative commentary is to discuss some aspects involved in depression. It is increasingly evident that the phenomenon of mood disorders, despite its unequivocal genetic origin, slips into a multifactorial set of biochemical and molecular events that involve the whole organism. A vast literature has provided evidence that recognizes changes in serotonergic neurotransmission in the pathophysiology of depression. In addition, an increased arachidonic acid/omega-3 fatty acid ratio, which confers to mammalian cell membranes their fluidity, is associated with the depressive state. The combination of the excessive expression of kinurenine and the increased fluidity of the membrane has never been considered in the meaning of a simultaneous effect in the determinism of the depressive condition. Furthermore, various evidence supports the relationship between intestinal microbiota and depression and confirms alterations in the microbiota in depressive pathology. typtophan; serotonin; depression; membrane fluidity; arachidonic acid; intestinal microbiota +
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Furthermore, proinflammatorycytokines increase monoamine reuptake by further reducing 5-HT levels [7; 8; 9]. In the 1970s and 1980s, a further element to the evaluation of the reduced presence of 5-HT in the depressive condition was added by some authors with reference to the similarity between neurons and platelets in relation to finding a reduced amount of 5-HT in the neurons and the platelets in the depressive condition [10; 11; 12; 13; 14; 15; 16; 17]. In more recent years, the results obtained by other authors through blood platelet fatty acids, in the interpretation of an artificial neural network, have enabled the possibility of carrying out a precise diagnostic evaluation of the two main psychopathologies, namely major depression (MD) and bipolar disorder (BD) [18; 19; 20]. Whereas 5-HT is mostly known for its role in mood, anxiety, psychosis, or memory in the central nervous system (CNS), more than 95% of total body 5-HT is present in the periphery. In addition, the majority of peripheral 5-HT is stored in platelets. On the other hand, platelets do not synthesize 5-HT, but they adsorb it from plasma through the 5-HT transporter and release it during their activation [21]. Actually, the function of 5-HT in platelets is not clear yet; studies suggest that it is important for the serotonin of the proteins necessary in platelet aggregation [22]. A recent study revealed platelet contributions to inflammation in reactions involving antigen-antibody complexes [23]. Furthermore, some studies have found a significant correlation between the abnormal membrane fluidity of platelets and the severity of dementia [24; 25; 26]. Platelets and neurons are unquestionably different cells, however, they share common characteristics in molecular organization and in protein composition [27]. In particular, various proteins are typically expressed in both neurons and platelets, and circulating platelets have been proposed as an alternative model to investigate neuronal dysfunctions and as an accessible peripheral biomarker to monitor the onset and the progression of neurological diseases. In this respect, some studies have reported platelet alterations in autism spectrum disorders [28]. The hypothesis that is formulated refers to the possibility of using the platelet as a diagnostic element in psychopathology [29] and in accordance with [PERSON] et al. [30]. The focus is on the role of membrane fluidity in the management of 5-HT uptake. The cell membrane is known to live in a  
Figure 1: Metabolic pathways of tryptophan. state of continuous mobility. Its fluidity is affected by the ratio of phospholipids to free cholesterol. In particular, long chain fatty acids, specifically arachidonic acid (AA) and docosahexaenoic acid (DHA), are integral components of neural membrane phospholipids and are extremely important for the maintenance of the optimum membrane fluidity of neurons [31].