摘要目的：探讨环腺苷二磷酸核糖（cyclic adenosine diphosphate ribose，cADPR）协同热刺激对小鼠下丘脑催产素神经细胞内钙离子浓度变化的调节作用。方法提取小鼠下丘脑视上核进行体外催产素神经元培养，胞外给予cADPR并伴随不同温度梯度（以2℃的梯度差分别将目标温度设置为28、34、37和39℃）及抑制剂（Ryanodine，8?bromo?cADPR，2?APB）的条件下，利用钙离子荧光成像系统检测胞浆内钙离子浓度的变化情况。另外，通过胞外给予催产素的刺激进而检测热敏感神经元胞浆内钙离子浓度的变化情况。结果细胞外给予100μmol/L cADPR并且伴随升温至37℃时，胞内钙离子浓度增加，39℃时升高更为明显，与胞内Ca2+基础相比较分别升高达125%和151%（P<0.05）。在相同条件下，腺苷二磷酸核糖和烟酰胺腺嘌呤二核苷酸诱发的胞内钙离子浓度升高现象类似于cADPR，但程度较弱。瞬时受体电位M2通道阻滞剂2?APB可显著阻断以上反应。100 nmol/L催产素的刺激可以使热敏感神经元胞内出现一种相对平缓且持续的Ca2+升高。结论热温度依赖的环腺苷二磷酸核糖/瞬时受体电位M2介导的钙内流是调控催产素神经元胞内钙离子浓度升高的机制，有利于催产素的分泌。

abstractsObjective To investigate the intracellular calcium concentration([Ca2+]i)in mouse hypothalamic oxytocin neurons co?regulated by cyclic adenosine diphosphate ribose(cADPR)and thermal stimulation. Methods Oxytocin neurons were separated from supraoptic nucleus of mice and cultured in vitro. Under different temperature gradients (with a temperature gradient of 2 degrees Celsius and target temperatures set to 28,34,37 and 39 degrees Celsius),the neurons were treated with extracellular cADPR and inhibitors(Ryanodine,8?bromo?cADPR,2?APB). Calcium fluorescence imaging system was used to detect[Ca2+]i). In addition,the change in[Ca2+]i)in the heat?sensitive neurons were measured after stimulation of extracellular oxytocin. Results An increased in[Ca2+]i with 100μmol/L extracellular cADPR was noted when the temperature was raised to 37 degrees Celsius,and became even more significant when the temperature was raised to 39 degrees Celsius,corresponding to 125% and 151% times,respectively,the basic level of[Ca2+]i(P<0.05). Under the same conditions,adenosine diphosphate ribose and nicotinamide adenine dinucleotide may also induce similar changes in[Ca2+]i as did cADPR,but with weaker actions. These actions were obviously blocked by the transient receptor potential M2 channel(TRPM2)blocker 2?APB. 100 nmol/L oxytocin stimulation of the heat?sensitive neurons was noted to induce a relatively flat and&nbsp;steady increase in [Ca2+]i. Conclusion Temperature?dependent activity of cADPR/TRPM2?mediated calcium influx may underlie the regulation of increased[Ca2+]i in oxytocin neurons,which may contribute to production of oxytocin.