Effects of temperature on pacemaker potentials in the mouse small intestine
Effects of temperature on pacemaker potentials in the mouse small intestine
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DOI：
10.1007/s00424-006-0201-3
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发表时间：
2007-05-01
影响因子：
4.5
通讯作者：
Suzuki, Hikaru
中科院分区：
文献类型：
--
作者：
Kito, Yoshihiko;Suzuki, Hikaru
应用细胞内记录技术研究了温度对分布于小鼠小肠的Cajal肌间质细胞（ICC-MY）起搏电位产生的影响。在26-40 ℃范围内，随着温度的升高，起搏电位的频率和最大上升速率（dV/dt（max））增加，而其持续时间减少。静息膜电位和起搏电位幅度不受温度变化的影响。温度升高降低了起搏电位之间的间隔期间自发产生的单一电位的幅度、持续时间和上升时间。代谢抑制剂（KCN和碘乙酸）降低起搏电位的频率，但对振幅和dV/dt（max）无影响。Cyclopiazonic acid（3 μ M），一种内部钙泵的抑制剂，在低温条件下（< 29 ℃）消除了起搏电位，但在高温条件下（> 38 ℃）没有。这些结果表明，起搏电位的主要和平台组件具有不同的温度敏感性：主要组件是高度的温度敏感性，并在较高的温度下被激活，而平台组件是由温度不敏感的机制激活形成的。这些结果还表明，ESTA诱导的细胞内Ca 2+处理系统似乎参与启动的起搏电位的产生，但不是在他们的配置。
The effects of temperature on the generation of pacemaker potentials recorded from myenteric interstitial cells of Cajal (ICC-MY) distributed in the mouse small intestine were investigated using intracellular recording techniques. In response to increasing temperatures in the range of 26-40 degrees C, the frequency and maximum rate of rise (dV/dt (max)) of pacemaker potentials were increased while their duration was decreased. The resting membrane potential and amplitude of the pacemaker potentials were not affected by change in temperature. Elevation of temperature decreased the amplitude, duration, and rise time of unitary potentials generated spontaneously during intervals between the pacemaker potentials. Metabolic inhibition (KCN and iodoacetic acid) decreased the frequency of pacemaker potentials with no alteration to the amplitude and dV/dt (max). Cyclopiazonic acid (3 mu M), an inhibitor of the internal Ca2+ pump, abolished pacemaker potentials in low-temperature conditions (< 29 degrees C) but not at high-temperature conditions (> 38 degrees C). These results suggest that the primary and plateau components of pacemaker potentials have different temperature sensitivities: the primary component is highly temperature-sensitive and is activated at higher temperatures, while the plateau component is formed by activation of temperature-insensitive mechanisms. The results also suggest that the mitochondria-induced intracellular Ca2+ handling system seems to be involved in the initiation of the generation of pacemaker potentials but not in their configuration.