0023-6152

AA00697606

7443180

Marine harmful algal blooms (HABs) caused by the dinoflagellate Karenia mikimotoi frequently induce severe fish mortality through gill damage and respiratory dysfunction. While starvation is generally regarded as a physiological stressor, short-term fasting has been reported to enhance fish tolerance to acute HAB toxicity. In this study, we investigated the effects of temporary starvation on survival and brain monoaminergic responses in marine medaka (Oryzias javanicus) exposed to K. mikimotoi. Adult fish were assigned to either fed or 48-h starved conditions and subsequently exposed to K. mikimotoi (1.0 × 10⁴ cells mL⁻¹). Survival analysis demonstrated that starved fish survived markedly longer than fed fish, with the onset of mortality delayed by approximately 75 min. To explore the neurochemical mechanisms underlying this enhanced tolerance, brain concentrations of dopamine (DA), serotonin (5-HT), norepinephrine (NE), epinephrine (E), and their metabolites were quantified using high-performance liquid chromatography with electrochemical detection. As a result of the experiment, starved fish consistently exhibited lower concentrations of all measured monoamines and their metabolites in the non-exposed groups compared with fed fish, with the effect being more pronounced in the dopaminergic system. This overall tendency suggests broad suppression of dopaminergic, serotonergic, and noradrenergic activities under starvation conditions. In contrast, exposure to K. mikimotoi tended to increase the concentrations of these monoamines and their metabolites. However, even after exposure, starved fish generally maintained lower levels than fed fish for several compounds. Collectively, these findings suggest that short-term starvation induces a hypometabolic neurophysiological state characterized by reduced locomotor and respiratory activity, thereby suppressing oxygen consumption and delaying mortality. The present study highlights the potential role of the neuro-metabolic axis in mediating fish resilience against HAB toxicity and provides new insights into the neurophysiological mechanisms underlying starvation-induced tolerance to acute environmental stress.