Bramham C R, Southard T, Ahlers S T, Sarvey J M
Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799, USA.
Brain Res. 1998 Apr 13;789(2):245-55. doi: 10.1016/s0006-8993(97)01265-1.
Exposure to stress has previously been found to impair long-term potentiation (LTP) in the hippocampus. Exposure to stress has also been proposed to induce an LTP-like effect. We examined the effect of acute cold stress on synaptic transmission, neuronal excitability, and LTP induction in the medial perforant path-granule cell synapse of freely moving rats. After obtaining baseline recordings of evoked field potentials at room temperature (23 degrees C), rats were transferred to an environmental cage maintained at 4 degrees C (cold group) or 23 degrees C (control group) and, 90 min later, high-frequency stimulation (HFS) was applied to the medial perforant path. Serum corticosterone measured in trunk blood from rats without implanted electrodes was significantly elevated in cold exposed (28. 7 microg/dl) rats relative to control (6.6 microg/dl). Despite increased corticosterone levels indicative of stress activation, cold exposed rats exhibited LTP of the fEPSP slope and population spike of similar magnitude and time course as controls. In addition, there was no stress-specific effect on the fEPSP slope or population spike and no effect on paired-pulse plasticity. Surprisingly, despite extensive cage acclimation, transferring rats to the environmental cage was associated with a reduction in population spike amplitude and an enhancement in paired-pulse facilitation. The results show that acute cold stress leading to elevated serum corticosterone levels neither induces LTP-like increases in synaptic efficacy nor impairs tetanus-evoked LTP in the dentate gyrus of freely moving rats. Thus, impaired working memory during cold stress is not due to an inability of perforant path synapses to express LTP.
先前已发现，暴露于应激状态会损害海马体中的长时程增强（LTP）。也有人提出，暴露于应激状态会诱导类似LTP的效应。我们研究了急性冷应激对自由活动大鼠内侧穿通通路-颗粒细胞突触的突触传递、神经元兴奋性和LTP诱导的影响。在室温（23摄氏度）下获得诱发场电位的基线记录后，将大鼠转移至保持在4摄氏度的环境笼中（冷应激组）或23摄氏度的环境笼中（对照组），90分钟后，对内侧穿通通路施加高频刺激（HFS）。在未植入电极的大鼠的躯干血中测得的血清皮质酮，冷暴露大鼠（28.7微克/分升）相对于对照组（6.6微克/分升）显著升高。尽管皮质酮水平升高表明应激激活，但冷暴露大鼠的场兴奋性突触后电位（fEPSP）斜率和群体峰电位的LTP表现出与对照组相似的幅度和时间进程。此外，对fEPSP斜率或群体峰电位没有应激特异性影响，对双脉冲可塑性也没有影响。令人惊讶的是，尽管进行了广泛的笼内适应，但将大鼠转移至环境笼中与群体峰电位幅度降低和双脉冲易化增强有关。结果表明，导致血清皮质酮水平升高的急性冷应激既不会诱导类似LTP的突触效能增加，也不会损害自由活动大鼠齿状回中强直刺激诱发的LTP。因此，冷应激期间工作记忆受损并非由于穿通通路突触无法表达LTP。
