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Published on: October 29, 2014
Antibiotic exposure postweaning disrupts the neurochemistry and function of enteric neurons mediating colonic motor
Lin Y Hung1, Pavitha Parathan1, Prapaporn Boonma2,3,4
1Department of Physiology, University of Melbourne, Parkville, Victoria, Australia.
Insights
Antibiotic vancomycin given postweaning alters gut microbiota and slows colonic motility by affecting enteric nervous system (ENS) neurochemistry in mice. This highlights developmental-specific impacts of antibiotics on gut function.
Area of Science:
- Neuroscience
- Microbiology
- Gastroenterology
Background:
- Gut microbiota plays a crucial role in enteric nervous system (ENS) development during the weaning period.
- Microbiota-derived signals influencing ENS maturation are not fully understood.
- Antibiotic administration during critical developmental windows can impact gut function.
Purpose of the Study:
- To investigate the physiological effects of postweaning vancomycin administration on colonic motility and ENS neurochemistry.
- To characterize alterations in neuronal excitability and neurochemistry in response to antibiotic-induced microbiota shifts.
- To compare vancomycin's impact during the weaning period versus neonatal exposure.
Main Methods:
- Oral vancomycin administration to weaned mice.
- 16S rDNA sequencing to analyze fecal microbiota composition and diversity.
- Calcium (Ca2+) imaging in reporter mice to assess neuronal activity in the myenteric and submucosal plexuses.
- Assessment of colonic migrating motor complexes (CMMCs) and neurotransmitter levels.
Main Results:
- Vancomycin significantly altered gut microbiota composition, increasing Akkermansiaceae, Lactobacillaceae, and Enterobacteriaceae while decreasing Lachnospiraceae and Bacteroidaceae.
- Postweaning vancomycin exposure slowed CMMCs without altering mucosal serotonin levels.
- Neurochemical changes included reduced cholinergic and calbindin+ myenteric neurons, reduced neuronal nitric oxide synthase+ submucosal neurons, and altered neurofilament M+ neuron populations.
- Increased neuronal transmission and responsiveness were observed in both myenteric and submucosal neurons.
Conclusions:
- Postweaning vancomycin disrupts colonic motility by altering ENS neurochemistry, leading to slower CMMCs.
- The effects of vancomycin on the ENS and colonic motility are distinct between neonatal and weaning periods.
- These findings underscore the developmental stage-specific impact of antibiotics on the gut-brain axis.
Abstract:
The period during and immediately after weaning is an important developmental window when marked shifts in gut microbiota can regulate the maturation of the enteric nervous system (ENS). Because microbiota-derived signals that modulate ENS development are poorly understood, we examined the physiological impact of the broad spectrum of antibiotic, vancomycin-administered postweaning on colonic motility, neurochemistry of enteric neurons, and neuronal excitability. The functional impact of vancomycin on enteric neurons was investigated by Ca2+ imaging in Wnt1-Cre;R26R-GCaMP3 reporter mice to characterize alterations in the submucosal and the myenteric plexus, which contains the neuronal circuitry controlling gut motility. 16S rDNA sequencing of fecal specimens after oral vancomycin demonstrated significant deviations in microbiota abundance, diversity, and community composition. Vancomycin significantly increased the relative family rank abundance of Akkermansiaceae, Lactobacillaceae, and Enterobacteriaceae at the expense of Lachnospiraceae and Bacteroidaceae. In sharp contrast to neonatal vancomycin exposure, microbiota compositional shifts in weaned animals were associated with slower colonic migrating motor complexes (CMMCs) without mucosal serotonin biosynthesis being altered. The slowing of CMMCs is linked to disruptions in the neurochemistry of the underlying enteric circuitry. This included significant reductions in cholinergic and calbindin+ myenteric neurons, neuronal nitric oxide synthase+ submucosal neurons, neurofilament M+ enteric neurons, and increased proportions of cholinergic submucosal neurons. The antibiotic treatment also increased transmission and responsiveness in myenteric and submucosal neurons that may enhance inhibitory motor pathways, leading to slower CMMCs. Differential vancomycin responses during neonatal and weaning periods in mice highlight the developmental-specific impact of antibiotics on colonic enteric circuitry and motility.
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