MicrobiotaMi Comment 16_21  by Stefania Blasa

Related Journal Article:  Correlation of gut microbiota and neurotransmitters in a rat model of post-traumatic stress disorder.

This article was published in the: Journal of Traditional Chinese Medical Sciences,Volume 7, Issue 4, December 2020, Pages 375-385.  https://doi.org/10.1016/j.jtcms.2020.10.005

Post-traumatic stress disorder model shows changes in neurotransmitter production and gut microbiota composition

The gut microbiota has recently attracted large research attention due to its ability to regulate the brain-gut axis. The central nervous system regulates the function and homeostasis of the gastrointestinal tract, while gut microbiota could mediate inflammation, hormone synthesis and neurotransmitter production. A disturbance in this microbiota could affect several brain functions and could lead to cognitive and emotional impairment. In fact, disruption of gut microbiota has been associated with mental illnesses such as depression, anxiety and autism spectrum disorder, and is linked to degenerative diseases such as Parkinson and Alzheimer.

Post-traumatic stress disorder (PTSD) is an important condition that tipically develops after traumatic events such as war, earthquakes or violent crimes and has a large impact worldwide, especially in the Asia-Pacific region, in the United States and in Egypt. Several patients show emotional issues, depression or anxiety and drug abuse disorders, as well as suicidal and aggressive behaviours. Although human research in this field is at the moment limited, the study of the pathophysiology of this disorder could lead to new strategies for treatment and prevention. In previous studies, it has been demonstrated that anxiety and fear behaviours could affect the production of ϒ-aminobutyric acid (GABA) and its receptor content; moreover, anxiety and depression often accompany gastrointestinal diseases. In this paper, Zhou and colleagues explored the connection between the abundance and diversity of gut microbiota and neurotransmitter release in a single prolonged stress (SPS) rat model, which simulates symptoms of PTSD patients, such as anxiety, irritability, depression and fear behaviours.

Results showed that after exposure to SPS, Serotonine (5-TH) levels in the cerebral cortex significantly decreased. Since 5-TH is an inhibitory neurotransmitter, a low level suggests that rats were in a hyper-excited state. This was also confirmed by the increase of excitatory neurotransmitters such as Norepinephrine (NE) and Dopamine (DA). This indicated that SPS could disrupt the brain’s state of excitement-inhibition through changes in neurotransmitters content. Moreover, the gut microbiota profile in SPS models revealed that PSP might leading to changes in the microbial populations at different taxa levels. Results showed a great diversity in the microbial community of SPS rats and differences in the gut microbial structure compared to the control group. In particular, significant changes in the composition and abundance of Cyanobacteria and Proteobacteria were observed, suggesting that gut microbiota could be an essential regulator of neural functions and stress-related disorders.

Taken together, these data revealed that SPS models, which exhibit anxiety and fear behaviours, had decreased levels of 5-TH and increased levels of DA and NE as a sign of hyper-excitement state, and that the structure and abundance of Cyanobacteria, Proteobacteria and other microbial phyla underwent to significant changes compared to the control. Despite the research limitations in this field, this study could provide new mechanisms for future therapeutic research for PTSD treatment.

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<a href="https://microbiotami.com/author/stefania/" target="_self">Stefania Blasa</a>

Stefania Blasa

Stefania Blasa is a Postdoc in “Converging Technologies for Biomolecular Systems” at University of Milan-Bicocca; she is interested in neurophysiology and works on in-vitro neuronal differentiation induced by innovative technologies. During her master thesis, she worked on the simultaneous detection of mutations responsible of peripheral nerve system genetic diseases.