| | Neurotransmitters | Mechanism | References |
| | GABA | The primary inhibitory neurotransmitter of the central nervous system (CNS), GABA, is generated during the breakdown of glutamate. GABA is essential for controlling neuronal excitability. Anxiety and depression are two of the many chronic disorders whose pathogenesis has been linked to GABA system dysfunction. In culture, bacteria such as Lactobacillus and Bifidobacterium species can convert glutamate to GABA. The capacity of L. rhamnosus to alter the central expression of GABA receptors in significant CNS brain regions in mice provides additional proof that it may be useful in the treatment of anxiety and depression. The fact that some of the behavioral and physiological changes brought on by L. rhamnosus require the vagus nerve has led to the revelation that there is a functional communication link between bacteria, the stomach, and the brain. According to certain theories, bacteria may alter the GABA system and so affect the chemistry of the brain. | [32, 33] |
| | Brain-derived neurotrophic factor (BDNF) | The central nervous system is supported by the neurotrophin (protein) BDNF, which also encourages the creation and differentiation of new neurons and synapses (CNS). It is generally known that BDNF plays a role in neuronal differentiation, survival, and the growth and plasticity of synapses. It has been demonstrated that a number of antidepressants, among other treatments, can increase BDNF expression in the brain. Chronic depression has been linked to low levels of BDNF. It is crucial to emphasize that BDNF mRNA and protein levels have been linked to the gut-brain axis. Pathogen-free mice have demonstrated that intestinal microbiota increases levels of hippocampal BDNF after receiving antibiotics and fecal transplants. Trichurismuris infection was observed to reduce the amounts of BDNF mRNA in the hippocampus in mice; however, treatment with B. longum caused the levels of BDNF to be restored to normal. It has been shown that oral antibiotic treatment of specific pathogen-free animals, colonization of GF BALB/c mice with NIH Swiss mice, promotes exploratory behavior and BDNF expression. Conflicting conclusions about BDNF and connections between BDNF levels and anxiety-like behaviors have been drawn from studies using GF mice. Researchers discovered a link between the drop in BDNF levels and the decrease in anxiety in Swiss Webster, NMRI, and BALB/c male mice. However, two additional studies utilizing Swiss Webster female mice showed that BDNF levels varied, exhibiting both increases and declines. In addition to strain and sex, it is probable that other hormonal and/or experimental factors will change how the gut flora affects BDNF. For instance, the hypothesis that a mouse’s reaction to stress is impacted by its estrous cycle may help to explain the observed differences in BDNF expression between male and female mice. The timing and order of behavioral tests, the housing conditions for GF mice, and other variables might have had an impact on the BDNF findings. In view of the function BDNF plays in neuroplasticity and neurological illnesses, additional research is required to examine the interactions between BDNF and other neurotrophins as well as the circumstances in which these growth factors are impacted by the microbiome. | [34, 35] |
| | Serotonin | Serotonin is a unique monoamine neurotransmitter and plays a critical role in controlling nearly all brain functions. Anxiety and depression are two neuropsychiatric illnesses that have links to serotonergic system disorders. A few of the causes of dysfunction include insufficient serotonin production, a deficiency in serotonin receptor sites, or a barrier that prevents serotonin from reaching the receptor sites. It is noteworthy that enterochromaffin cells in the GI tract create about 90% of serotonin. Escherichia and Enterococcus species, which are typically found in the gut, can also create serotonin. Additionally, gut microorganisms can encourage the creation of serotonin by interacting with enterochromaffin cells via short-chain fatty acids. The ability of the CNS to operate may be directly impacted by the gut microorganisms that regulate serotonin production. For instance, compared to control animals that had naturally colonized the area, male germ-free (GF) mice displayed increased levels of serotonin and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), in the hippocampus. Furthermore, the plasma tryptophan concentrations were higher in the male GF mice, pointing to a putative humoral mechanism by which the gut microbiota may affect CNS serotonergic neurotransmission. Additionally, serotonin and 5-HIAA levels in adult GF mice were not increased by introducing bacteria from previously colonized animals into their microbiome. | [36, 37] |
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