Elevated temperature exacerbates glufosinate-ammonium-induced neurobehavioral toxicity in juvenile Eriocheir sinensis.

Under the combined pressures of global climate change and agrochemical pollution, the interactive risk of high temperature and pesticide exposure remains unclear. This 30-day chronic toxicity study systematically elucidated how high temperature exacerbates glufosinate-ammonium (GLA)-induced neurobehavioral toxicity in juvenile Eriocheir sinensis. The results showed that GLA exposure induced significant neurobehavioral abnormalities, including appendage tremors and hyperactivity, with temperature exerting non-monotonic modulation: moderate warming (26 °C) aggravated excitatory behaviors, while extreme high temperature (30 °C) inhibited locomotion due to exceeding physiological tolerance thresholds, reflecting nervous system failure rather than recovery. Mechanistically, high temperature potentiated GLA-induced oxidative stress, triggering the "oxidative stress-neuroinflammation-apoptosis" cascade which ultimately led to neurocyte apoptosis or neuronal damage, as validated by increased serum levels of neuron-specific enolase (NSE) and central nervous system specific protein β (S100β). Targeted metabolomics revealed that combined stress disrupted neurotransmitter homeostasis. Excitatory neurotransmitters L-glutamic acid and L-aspartic acid were significantly increased, inducing excitotoxicity, while compensatory GABA elevation failed to reverse neural excitation-inhibition imbalance. This study is the first to reveal the multi-pathway, multi-organ coordinated mechanism by which high temperature amplifies GLA's neurobehavioral toxicity, providing a critical scientific basis for pesticide ecological risk assessment under global warming.