A transient increase in temperature induces persistent potentiation of synaptic transmission in rat hippocampal slices.
A transient increase in temperature induces persistent potentiation of synaptic transmission in rat hippocampal slices.
复制标题
温度的短暂升高会诱导大鼠海马切片中突触传递的持续增强。
DOI：
10.1016/s0306-4522(00)00431-0
复制
发表时间：
2000
期刊：
影响因子：
3.3
通讯作者：
Dunwiddie,TV
中科院分区：
文献类型：
--
作者：
Masino,SA;Dunwiddie,TV
先前的研究表明，将大鼠海马脑切片的温度从32.5°C提高到38.5°C，会导致CA1区兴奋性突触传递的腺苷介导的显著减少。在这里，我们发现当温度降低到32.5°C时，场兴奋性突触后电位的振幅通常会恢复到一个相对于初始基线显著增强的水平。这种增强作用起效迅速（回到32.5°C后< 5min），持续时间长（温度升高结束后约60min）。单独加入腺苷不能诱导类似的作用，腺苷受体拮抗剂也不能阻断这种增强作用。因此，虽然腺苷介导的兴奋性突触传递减少发生在温度升高期间，但它与增强无关。同样，n -甲基-d-天冬氨酸受体激活也不需要，因为n -甲基-d-天冬氨酸受体拮抗剂不会影响这种形式的增强。综上所述，我们认为瞬时升高的脑切片温度代表了一种诱导海马突触可塑性的新方式，并可能为阐明参与功能可塑性的其他细胞机制提供范例。
Previous studies have shown that increasing the temperature of rat hippocampal brain slices from 32.5 to 38.5°C initiates a profound, adenosine-mediated decrease in excitatory synaptic transmission in the CA1 region. Here we found that upon lowering the temperature back to 32.5°C, the amplitude of the field excitatory postsynaptic potential often recovers to a level that is significantly potentiated with respect to the initial baseline. This potentiation is rapid in onset (< 5min following return to 32.5°C) and long lasting (>60min following the termination of the increase in temperature). Similar effects could not be induced by superfusion with adenosine alone, and adenosine receptor antagonists did not block the potentiation. Therefore, although an adenosine-mediated decrease in excitatory synaptic transmission occurs during the temperature increase, it is unrelated to the potentiation. Likewise, N-methyl-d-aspartate receptor activation is not required, as N-methyl-d-aspartate receptor antagonists do not influence this form of potentiation. In summary, we propose that transiently increasing brain slice temperature represents a novel way to induce synaptic plasticity in the hippocampus, and may provide a paradigm to elucidate additional cellular mechanisms involved in functional plasticity.