Sublethal Ammonia Exposure Suppresses Neurotransmitters, Impairing Zebrafish Embryo Locomotion and Behavior

Ammonia is a widespread environmental pollutant and a potent neurotoxicant in aquatic environments. While adult teleosts can adapt to stressors, embryos are particularly vulnerable due to incomplete organogenesis and developing blood-brain barriers, limiting their acclimation strategies. Despite this, the specific behavioral and neurochemical responses of early-stage embryos to ammonia exposure have remained poorly understood compared to adult fish, representing a critical gap in understanding developmental neurotoxicity.

This study exposed zebrafish embryos to sublethal concentrations of NH₄Cl for 96 h. Researchers assessed various behavioral endpoints, including spontaneous locomotion, light-dark preference, touch-evoked escape responses, and feeding behavior. Gene expression analysis was performed using RT-qPCR to quantify transcripts of key neurotransmitters and related enzymes, comparing exposed embryos to unexposed controls to identify neurochemical alterations.

Exposure to sublethal ammonia concentrations induced significant neurobehavioral deficits in zebrafish embryos. They exhibited reduced spontaneous locomotion, disrupted light-dark preference, diminished touch-evoked escape responses, and impaired feeding behavior. Furthermore, RT-qPCR analysis revealed marked decreases in the transcripts of several crucial neurotransmitters and related enzymes. These included oxytocin, vasopressin, tyrosine hydroxylase, choline acetyltransferase, and glutamate decarboxylase. These findings collectively indicate a broad impact on both motor function and neurochemical signaling pathways.

Even nonlethal ammonia levels can induce coordinated neurobehavioral and neurotransmitter deficits during critical windows of vertebrate development.