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Gut-brain axis

Uni of Notts, Neurobiology of Disease, year 2, topic 18

TermDefinition
Gut-brain axis Bidirectional communication connecting central & enteric nervous systems while linking emotional/cognitive pathways with peripheral intestinal function
Intestinal neural composition & connectivity Contains roughly 500 million neurons utilizing diverse neurotransmitters & neuropeptides to communicate with the brain, spinal cord, ANS, & HPA axis
Primary chemical communication vectors Communicates through neurotransmitters, short-chain fatty acids, indoles, catechols, & specific microbial metabolites
Behavioral markers in germ-free animals Show altered neurotransmitter expression/turnover, causing impaired social behavior, exaggerated HPA reactions, & heightened motor/sexual activities. Can be restored with exposure to species specific bacteria
Gut-first afferent signaling conduits Sends sensory inputs from the GI tract up to the central nervous system via spinal & vagus pathways
Efferent central nervous system signals Connects to gut walls to control motility, permeability, local immune activation, & enteroendocrine signaling
Pathological risk of gut dysbiosis Aberrant shifts in gut microbiota structure can actively prompt psychiatric & neurodegenerative disorders. Can lead to both IBS & emotional distress
Microbiome size & classification parameters Features bacteria, viruses, fungi, yeast, & phages across 1,000 species, totaling 10^14 cells & weighing over 1kg
Bacterial strains & related neurotransmitters Lactobacillus yields ACh, GABA, & BDNF; Candida/Strep/E. coli produce ~90% of serotonin; Serratia/Bacilli synthesize dopamine
Bifidobacterium brain impact Probiotic strains elevate hippocampal brain-derived neurotrophic factor levels to support local neurogenesis
Short-chain fatty acids central targets Microbial short-chain fatty acids directly alter baseline neuroinflammation & central neurogenesis pathways through gut-brain signalling pathways & reduce glial overactivation
Endocrine regulation of gut motility 5-HT & GLP-2 accelerate emptying; SST, GLP-1, PPY, GIP, & CCK decrease motility, food intake, & pancreatic secretions
Environmental stress integration with gut-brain axis model riggers hypothalamic CRH secretion, combining hormones & neurotransmitters to modulate local intestinal effector cells
Developmental GBA physiological markers Initial microbiota shapes myelination, microglia function, neuroinflammation, BBB structural integrity, & alpha-synuclein dynamics
Intestinal environmental heterogeneity Microclimates differ in local pH, oxygenation, antimicrobial peptide expression, & bile salt levels, affecting microbial density
Metabolite downstream delivery systems Activates enteroendocrine cells to prompt systemic hormone release or directly stimulates the vagus nerve
Leaky-gut pathology consequences Disrupted epithelial barriers impair normal endocrine & vagal transmission from the lumen to the brain
Age-related microbiome shifts Aging reduces protective bacterial group 1 while inflating opportunistic bacterial groups 2 & 3
Pathological markers of group 2 expansion Elevates systemic inflammatory lipopolysaccharide (LPS), increasing overall vulnerability to Alzheimer's disease
High-fat diet neurodegenerative correlations Modifies the microbiome matrix to augment toxic amyloid-beta deposition inside the hippocampus
Targeted antibiotic & probiotic applications Restores normal microbial distribution to limit neurodegenerative onset or delay Alzheimer's disease progression
Fecal microbiota transplant mechanisms Counteracts senescent behavioral decline, drops hippocampal neutrophil density, & reverses Alzheimer's phenotypes in vivo
Neurotransmitter molecules produced by microbiome 5-HT, dopamine, ACh, GABA, histamine, melatonin, nitrite & nitrate (to synthesise NO)
Prebiotic & probiotic dietary shifting Dietary interventions inflate beneficial phyla like Bifidobacterium & Lactobacillus, shifting the microbiome toward heavy production of protective short-chain fatty acids
High-fat diet & hippocampal amyloid-beta Diets heavy in saturated fat favours opportunistic gram-negative bacteria with LPS on their membranes which can be translocated to the brain, causing inflammation & burdening amyloid clearance
Created by: Denny12
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