Brain cooling marginally increases acute thermal tolerance in Atlantic cod

The physiological mechanisms determining thermal limits in fishes are debated but remain elusive. It has been hypothesised that loss of motor function observed as a loss of equilibrium during an acute thermal challenge is due to direct thermal effects on brain neuronal function. To test this hypothesis, we mounted cooling plates on the head of Atlantic cod (<i>Gadus morhua</i>) and quantified whether local cooling of the brain increased whole-organism upper thermal tolerance (CT_max). Brain cooling reduced brain temperature by 2–6°C and increased CT_max by 0.5–0.7°C relative to instrumented and uninstrumented controls, suggesting that direct thermal effects on brain neurons might contribute to setting upper thermal limits in fish. However, the improvement in CT_max with brain cooling was small relative to the difference in brain temperature, demonstrating that other mechanisms (e.g. failure of spinal and peripheral neurons, or muscle) may also contribute to controlling acute thermal tolerance in fishes.

决定鱼类热耐受极限的生理机制至今仍存在争议，且尚未完全阐明。有假说提出，在急性热应激过程中出现的运动功能丧失（即平衡失调），是热直接作用于大脑神经元功能所致。为验证该假说，本研究将冷却板安装于大西洋鳕（*Gadus morhua*）头部，通过定量分析探究大脑局部降温是否会提升个体的临界高温耐受上限（CT_max）。与安装了测量装置及未安装装置的对照组相比，脑部降温可使脑温降低2~6℃，同时使CT_max提升0.5~0.7℃，这表明大脑神经元受到的直接热作用可能参与设定鱼类的高温耐受上限。但相较于脑温的变化幅度，脑部降温对CT_max的提升幅度较小，这表明其他机制（如脊髓与外周神经元功能障碍或肌肉功能异常）同样可能参与调控鱼类的急性热耐受能力。