serotonin

Overview

Serotonin, also known as 5-hydroxytryptamine (5-HT), is a biogenic monoamine that functions as a neurotransmitter, neuromodulator, and peripheral signaling molecule. It is synthesized from tryptophan through tryptophan hydroxylase-dependent pathways and is metabolized to 5-hydroxyindoleacetic acid (5-HIAA). In the central nervous system, serotonin helps regulate mood, anxiety, cognition, sleep, appetite, and pain processing, while in the gastrointestinal tract it contributes to motility and secretion. It also participates in platelet function and broader neuroimmune and gut-brain axis signaling.

In biomedical research, serotonin is often studied together with related pathways such as dopamine, glutamate, GABA, Indoleamine 2,3-dioxygenase 1, monoamine oxidase, and the NLRP3 inflammasome. Altered serotonin signaling is implicated in depression, migraine, constipation, neurodegenerative disease, and drug-induced neurotoxicity. Because of this broad physiological reach, serotonin is frequently used as a mechanistic readout in studies of host-microbe interactions, oxidative stress, mitochondrial dysfunction, and neurotransmitter imbalance.

Focus of Latest Publications

Recent publications have examined serotonin in several distinct biomedical contexts, most often as a readout of serotonergic signaling rather than as a direct therapeutic target. In neurobiology, a paper-based electrochemical aptasensor was developed to simultaneously detect dopamine and serotonin in human brain samples, with the goal of distinguishing healthy from Alzheimer’s disease tissue based on altered neurotransmitter levels. The assay used aptamer-mediated recognition and potential-resolved electrochemical discrimination to quantify both analytes on a single disposable electrode, supporting multiplexed neurochemical monitoring.

Several studies linked serotonin-related measures to gut-brain and stress-related biology. In neonatal mice exposed to maternal separation, changes in breast milk fatty acid composition were associated with altered gut microbiota, serum metabolites, and serotonin-related gene expression in the prefrontal cortex. Specifically, maternal separation was associated with elevated myristic acid in breast milk, reduced Akkermansia muciniphila in offspring, and decreased Tph2 and Htr1b expression in the prefrontal cortex; inosine supplementation selectively increased Htr1a expression. In a separate chronic restraint stress model, the polysaccharide PSLP-1 from Polygonatum sibiricum stems and leaves reduced depressive-like behaviors and was associated with restoration of tryptophan metabolism, including promotion of tryptophan hydroxylase-related 5-hydroxytryptamine synthesis, alongside gut microbiota remodeling.

Other recent work used serotonin as a biochemical marker in disease models. In Parkinson’s disease, sulforaphane treatment improved motor performance and dopaminergic neuron survival while normalizing the 5-HIAA/5-HT ratio in the striatum, alongside effects on the CBS-H2S axis, mitophagy, and NLRP3 inflammasome activation. In lung neuroendocrine neoplasms, tumor tissue was evaluated for serotonin expression as part of a broader hormone-secretion analysis; however, serotonin expression did not correlate with elevated 5-HIAA, whereas hormone secretion overall was associated with poorer survival. Finally, a rat brain study testing endogenous N,N-dimethyltryptamine reported no detectable endogenous DMT pool and little evidence that exogenous DMT was retained in serotonin terminals, arguing against a major serotonergic storage role for DMT in that model.