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The gut–brain axis is a bidirectional communication system that connects the gastrointestinal tract and the brain. This interaction is mediated through multiple pathways, including the vagus nerve, hormonal signals, immune responses, and chemical messengers produced by gut microbes.Microbial Contributions to Brain FunctionGut microbiota contributes significantly to brain function by producing neuroactive compounds. These include neuroactive compounds that influence neurotransmitters such...
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Related Experiment Video

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Investigating Alterations in Caecum Microbiota After Traumatic Brain Injury in Mice
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An Interplay Between Hypothalamic Microstructure, Systemic Metabolism and Gut Microbiome Composition in Male Rats at

Palkin Arora1,2, Megha Kumari1,3, Kavita Singh1

  • 1Radiological, Nuclear and Imaging Sciences (RNAIS), Institute of Nuclear Medicine and Allied Sciences (INMAS), DRDO, Delhi, India.

Journal of Neuroscience Research
|April 1, 2025
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Summary

Traumatic brain injury (TBI) alters metabolism and gut microbiome. Mild TBI causes hypermetabolism, while moderate TBI shows hypometabolism, impacting the hypothalamus-pituitary-adrenal (HPA) axis differently based on severity.

Keywords:
diffusion tensor imaginggut microbiomehypothalamusinflammationmetabolomicstraumatic brain injury

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Area of Science:

  • Neuroscience
  • Metabolomics
  • Microbiome research

Background:

  • Traumatic brain injury (TBI) is a significant insult affecting brain and systemic physiology.
  • Early metabolic and physiological changes following TBI are not fully understood.
  • The interplay between brain injury, metabolic shifts, and gut microbiome dysbiosis requires further investigation.

Purpose of the Study:

  • To investigate early brain and systemic physiological changes induced by mild and moderate TBI in male rats.
  • To explore the impact of TBI severity on metabolic profiles, hypothalamic structure, and the gut microbiome.
  • To elucidate the crosstalk between the hypothalamus-pituitary-adrenal (HPA) axis, metabolism, and gut microbiome post-TBI.

Main Methods:

  • Induction of mild and moderate TBI in male rats.
  • Serum and urine metabolic fingerprinting using metabolomics.
  • Hypothalamus structure assessment via diffusion tensor imaging (DTI).
  • Measurement of serum corticosterone and TNF-α levels.
  • Gut microbiome analysis, including Firmicutes: Bacteroidetes ratio.

Main Results:

  • Mild TBI rats exhibited a hypermetabolic response with increased serum and urine metabolites.
  • Moderate TBI rats showed decreased serum metabolites (lactate, pyruvate, amino acids) and altered urine profiles.
  • TBI induced hypothalamic structural changes, suggesting HPA axis disruption, and increased TNF-α in moderate TBI.
  • Gut microbiome dysbiosis was observed, characterized by an increased Firmicutes: Bacteroidetes ratio.
  • Distinct metabolic and physiological responses were noted between mild and moderate TBI groups.

Conclusions:

  • TBI significantly impacts systemic metabolism and gut microbiome composition.
  • Hypothalamic structure and HPA axis regulation are altered post-TBI, with severity-dependent effects.
  • A complex interplay exists between the HPA axis, metabolism, and gut microbiome following TBI.
  • Injury severity is a critical factor influencing the TBI-induced physiological response, necessitating phenotype-specific assessment.