Rapid temperature changes induce adenosine-mediated depression of synaptic transmission in hippocampal slices from rats (non-hibernators) but not in slices from golden hamsters (hibernators)
Rapid temperature changes induce adenosine-mediated depression of synaptic transmission in hippocampal slices from rats (non-hibernators) but not in slices from golden hamsters (hibernators)
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DOI：
10.1016/s0306-4522(98)00011-6
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发表时间：
1998-09-01
期刊：
影响因子：
3.3
通讯作者：
Igelmund, P
中科院分区：
文献类型：
--
作者：
Gabriel, A;Klussmann, FW;Igelmund, P
在意外体温过低的情况下，由快速温度变化引起的神经元通讯紊乱是一种危险，对于冬眠者来说，从冬眠中醒来是致命的。因此，我们研究了快速温度变化对金仓鼠（冬眠）和大鼠（非冬眠）海马切片突触诱导的CA1种群峰值的影响。温度以0.3℃/min的坡度变化，这与金仓鼠从冬眠中醒来时的体温上升相对应。在35 ~ 10 ~ 15℃的冷却过程中，仓鼠和大鼠切片的种群峰值振幅增大，分别在25 ~ 30℃和20 ~ 25℃达到最大值，然后随着冷却的进一步降低。在重新加热期间，仓鼠切片显示出与冷却期间相同的温度依赖性。相反，在大鼠切片中，温度变化发生了动态效应。与冷却相比，再加热时峰值振幅的强烈下降最为明显。在26-29摄氏度以上，抑郁与兴奋效应叠加在一起。茶碱（100-200 μ M）对这种抑制有很大的减弱作用，这可能是由于内源性腺苷浓度的增加，而内源性腺苷浓度的增加可能是增温过程中能量代谢失衡的结果。与大鼠切片相比，仓鼠切片对腺苷的敏感性较低，这可以解释仓鼠切片缺乏与变暖相关的抑郁。此外，代谢平衡对快速温度变化的较好抵抗可能会阻止仓鼠海马内源性腺苷的大量升高。对于冬眠动物来说，避免温度变化引起的神经元通讯干扰可能是从冬眠中安全唤醒的先决条件。(c) 1998 ibro。Elsevier Science Ltd.出版。
Disturbances in neuronal communication induced by rapid temperature changes are a risk in the context of accidental hypothermia and would be fatal for hibernators during arousal from hibernation. Therefore, we investigated the effects of rapid temperature changes on synaptically induced CA1 population spikes in hippocampal slices from golden hamsters (hibernators) and rats (non-hibernators). Temperature was changed ramp-like by 0.3 degrees C/min, which corresponds to the rise of body temperature in golden hamsters during arousal from hibernation. During cooling from 35 to 10-15 degrees C, the population spike amplitude increased, reached maximal values at 25-30 degrees C and 20-25 degrees C in hamster and rat slices, respectively, and then decreased with further cooling. During rewarming, hamster slices displayed the same temperature dependence as during cooling. In contrast, in rat slices dynamic effects of the temperature change occurred. These were most obvious in a strong depression of the spike amplitude during rewarming as compared to cooling. Above 26-29 degrees C, the depression was superimposed by an excitatory effect. The depression was largely attenuated by theophylline (100-200 mu M) and thus seems to be based on an increase of the concentration of endogenous adenosine, which in turn may result from an imbalance in energy metabolism during warming.The lack of warming-related depression in hamster slices can be explained by a lower sensitivity for adenosine as compared to rat slices. In addition, a better resistance of metabolic balance against rapid temperature changes may prevent large elevations of endogenous adenosine in the hamster hippocampus. For hibernators, the avoidance of temperature change-induced disturbances of neuronal communication may be a prerequisite for safe arousal from hibernation. (C) 1998 IBRO. Published by Elsevier Science Ltd.