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目前仍存在争议，且尚未完全阐明。有假说认为，急性热应激下出现的平衡丧失所表现出的运动功能丧失，是由于大脑神经元功能受到直接热效应影响所致。为验证该假说，我们将冷却板安装在大西洋鳕鱼（*Gadus morhua*）的头部，并量化了大脑局部降温是否会提升整体生物体的高温耐受极限（CT_max）。与安装了测量仪器的对照组和未安装仪器的对照组相比，脑部降温使脑温降低了2~6℃，并使CT_max提升了0.5~0.7℃，这表明大脑神经元受到的直接热效应可能参与决定鱼类的高温耐受极限。然而，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（例如脊髓与外周神经元功能衰竭或肌肉功能异常）也可能参与调控鱼类的急性热耐受能力。