Abstract：
Cellular temperature affects every biochemical reaction, underscoring its critical role in cellular functions. In neurons, temperature not only modulates neurotransmission but is also a key determinant of neurodegenerative diseases. Considering that the brain consumes a disproportionately high amount of energy relative to its weight, neural circuits likely generate a lot of heat, which can increase cytosolic temperature. However, the changes in temperature within neurons and the mechanisms of heat generation during neural excitation remain unclear. In this study, we achieved simultaneous imaging of Ca2+ and temperature using the genetically encoded indicators, B-GECO and B-gTEMP. We then compared the spatiotemporal distributions of Ca2+ responses and temperature. Following neural excitation induced by veratridine, an activator of the voltage-gated Na+ channel, we observed an approximately 2 °C increase in cytosolic temperature occurring 30 s after the Ca2+ response. The temperature elevation was observed in the non-nuclear region, while Ca2+ increased throughout the cell body. Moreover, this temperature increase was suppressed under Ca2+-free conditions and by inhibitors of ATP synthesis. These results indicate that Ca2+-induced upregulation of energy metabolism serves as the heat source during neural excitation.
摘要：
细胞温度影响每个生化反应,强调其在细胞功能中的关键作用。在神经元中，温度不仅调节神经传递，而且是神经退行性疾病的关键决定因素。考虑到大脑相对于其重量消耗不成比例的大量能量，神经回路可能会产生大量的热量，可以增加细胞溶质温度。然而,神经元内温度的变化和神经兴奋过程中热的产生机制尚不清楚。在这项研究中,我们使用基因编码的指标实现了Ca2+和温度的同时成像，B-GECO和B-gTEMP。然后，我们比较了Ca2响应和温度的时空分布。在维拉替丁诱导的神经兴奋后，电压门控Na+通道的激活剂，我们观察到Ca2反应后30s的胞浆温度升高约2°C。在非核区域观察到温度升高，而Ca2+在整个细胞体中增加。此外，在无Ca2条件下和ATP合成抑制剂抑制了这种温度升高。这些结果表明，在神经兴奋期间，Ca2诱导的能量代谢上调是热源。
