Prolonged Micromolar Ketamine Exposure Induces Dorsal Spinal Neuron Apoptosis and Locomotor Deficits During Early Development: Insights From FRET‐Based Sensor Zebrafish
In vivo experimental study reveals ketamine triggers spinal apoptosis and movement deficits in zebrafish, highlighting neurodevelopmental risks.
Key Points
To evaluate whether prolonged exposure to micromolar ketamine induces transient neuronal apoptosis and functional motor deficits during early neurodevelopment.
Engineered transgenic zebrafish stably expressing a genetically encoded fluorescence resonance energy transfer (FRET)-based biosensor in the nervous system to detect in vivo neuronal apoptosis.
Exposed zebrafish to micromolar ketamine concentrations (50 and 100 μM) for prolonged durations (48 and 72 h).
Evaluated functional locomotion impairments using high-throughput swimming tracking analysis.
Prolonged exposure to 50 and 100 μM ketamine for 48 and 72 hours induced discrete, consistent apoptosis specifically in developing primary sensory neurons and interneurons at the dorsal edge of the spinal cord.
High-throughput tracking demonstrated significant functional deficits, evidenced by marked reductions in maximum acceleration and velocity following ketamine exposure.