Arginine vasopressin (AVP) plays a hypothermic regulatory role in thermoregulation and is an important endogenous mediator in this mechanism. In the preoptic area (POA), AVP increases the spontaneous firing and thermosensitivity of warm-sensitive neurons and decreases those of cold-sensitive and temperature-insensitive neurons. Because POA neurons play a crucial role in precise thermoregulatory responses, these findings indicate that there is an association between the hypothermia and changes in the firing activity of AVP-induced POA neurons. However, the electrophysiological mechanisms by which AVP controls this firing activity remain unclear. Therefore, in the present study, using in vitro hypothalamic brain slices and whole-cell recordings, we elucidated the membrane potential responses of temperature-sensitive and –insensitive POA neurons to identify the applications of AVP or V_1a vasopressin receptor antagonists. By monitoring changes in the resting potential and membrane potential thermosensitivity of the neurons before and during experimental perfusion, we observed that AVP increased the changes in the resting potential of 50% of temperature-insensitive neurons but reduced them in others. These changes are because AVP enhances the membrane potential thermosensitivity of nearly 50% of the temperature-insensitive neurons. On the other hand, AVP changes both the resting potential and membrane potential thermosensitivity of temperature-sensitive neurons, with no differences between the warm- and cold-sensitive neurons. Before and during AVP or V_1a vasopressin receptor antagonist perfusion, no correlation was observed between changes in the thermosensitivity and membrane potential of all neurons. Furthermore, no correlation was observed between the thermosensitivity and membrane potential thermosensitivity of the neurons during experimental perfusion. In the present study, we found that AVP induction did not result in any changes in resting potential, which is unique to temperature-sensitive neurons. The study results suggest that AVP-induced changes in the firing activity and firing rate thermosensitivity of POA neurons are not controlled by resting potentials.

精氨酸加压素（AVP）在体温调节中发挥低温调节作用，是重要的内源性介质在这个机制中。在视前区（POA），AVP 增加热敏感神经元的自发放电和热敏感性，并减少冷敏感和温度不敏感神经元的自发放电和热敏感性。由于 POA 神经元在精确的体温调节反应中发挥着至关重要的作用，这些发现表明低温与 AVP 诱导的 POA 神经元放电活动的变化之间存在关联。然而，AVP 控制这种放电活动的电生理机制仍不清楚。_{因此，在本研究中，利用体外下丘脑脑切片和全细胞记录，阐明了温度敏感和不敏感 POA 神经元的膜电位反应，以确定 AVP 或 V 1a}的应用加压素受体拮抗剂。通过监测实验灌注前和实验期间神经元静息电位和膜电位热敏感性的变化，我们观察到 AVP 增加了 50% 温度不敏感神经元的静息电位变化，但减少了其他神经元的静息电位变化。这些变化是因为AVP增强了近50%的温度不敏感神经元的膜电位热敏感性。另一方面，AVP 改变温度敏感神经元的静息电位和膜电位热敏感性，而热敏感神经元和冷敏感神经元之间没有差异。_{AVP 或 V 1a}之前和期间加压素受体拮抗剂灌注后，所有神经元的热敏感性和膜电位的变化之间没有观察到相关性。此外，在实验灌注过程中，没有观察到神经元的热敏感性和膜电位热敏感性之间的相关性。在本研究中，我们发现 AVP 诱导不会导致静息电位的任何变化，这是温度敏感神经元所特有的。研究结果表明，AVP 引起的 POA 神经元放电活动和放电速率热敏感性的变化不受静息电位控制。