Antibiotic in Water Causes Anxiety in Zebrafish by Disrupting Gut Bacteria and Peptide Signaling

Zebrafish exposed to the antibiotic enrofloxacin at environmentally realistic levels (60 μg/L for 28 days) developed anxiety-like behaviors in two standard behavioral tests. The antibiotic disrupted the gut microbiome by increasing Bacteroidetes and lowering the Firmicutes/Bacteroidetes ratio, while significantly altering multiple peptide signaling molecules: intestinal GLP-1, 5-HT, IL-6, and TNF-α were elevated, plasma ACTH and cortisol were reduced, and brain levels of CRH, BDNF, and neuropeptide Y were increased — suggesting the microbiota-gut-brain axis mediated the behavioral changes.

Zebrafish were exposed to enrofloxacin at 6 and 60 μg/L for 28 days. Anxiety-like behavior was measured using light-dark test and novel tank task. Gut microbiome composition was analyzed. Intestinal, plasma, and brain levels of multiple peptides and signaling molecules were measured.

This study shows how environmental antibiotic contamination can disrupt gut bacteria in ways that alter peptide hormone signaling throughout the body and brain, ultimately changing behavior. It highlights the interconnectedness of the microbiome, gut peptides like GLP-1, and brain neuropeptides like NPY in regulating mood and anxiety.

This research adds to the growing evidence that gut bacteria communicate with the brain through peptide hormones. It demonstrates that environmental disruptions to the microbiome — even from low-level antibiotic exposure — can ripple through the entire peptide signaling network, affecting GLP-1 in the gut, stress peptides in the blood, and neuropeptides in the brain. This has implications for understanding how environmental toxins might contribute to anxiety and mood disorders.

Zebrafish study — results may not directly translate to humans. The antibiotic used (enrofloxacin) is primarily veterinary. Correlation between microbiome changes and peptide alterations does not prove causation. Sample size not specified in abstract. No germ-free controls to confirm microbiome-mediated mechanism.