Department of Neurobiology and Physiology, Physiology and Behavior, University of California, Davis, California 95616, USA.
Am J Physiol Regul Integr Comp Physiol. 2011 Aug;301(2):R438-47. doi: 10.1152/ajpregu.00016.2011. Epub 2011 May 11.
Previous studies in hibernating species have characterized two forms of neural plasticity in the hippocampus, long-term potentiation (LTP) and its reversal, depotentiation, but not de novo long-term depression (LTD), which is also associated with memory formation. Studies have also shown that histamine injected into the hippocampus prolonged hibernation bout duration. However, spillover into the ventricles may have affected brain stem regions, not the hippocampus. Here, we tested the hypothesis that decreased brain temperature shifts the major function of the hippocampus in the Syrian hamster (Mesocricetus auratus) from one of memory formation (via LTP, depotentiation, and de novo LTD) to increasing hibernation bout duration. We found reduced evoked responses in hippocampal CA1 pyramidal neurons following low-frequency stimulation in young (<30 days old) and adult (>60 days old) hamsters, indicating that de novo LTD was generated in hippocampal slices from both pups and adults at temperatures >20°C. However, at temperatures below 20°C, synchronization of neural assemblies (a requirement for LTD generation) was markedly degraded, implying that de novo LTD cannot be generated in hibernating hamsters. Nonetheless, even at temperatures below 16°C, pyramidal neurons could still generate action potentials that may traverse a neural pathway, suppressing the ascending arousal system (ARS). In addition, histamine increased the excitability of these pyramidal cells. Taken together, these findings are consistent with the hypothesis that hippocampal circuits remain operational at low brain temperatures in Syrian hamsters and suppress the ARS to prolong bout duration, even though memory formation is muted at these low temperatures.
先前对冬眠物种的研究已经确定了海马体中的两种神经可塑性形式，长时程增强（LTP）及其逆转，去极化，但不是新的长时程抑制（LTD），后者也与记忆形成有关。研究还表明，向海马体中注射组胺会延长冬眠期。然而，这种物质可能会溢出到脑室中，从而影响脑干部位，而不是海马体。在这里，我们测试了一个假设，即大脑温度的降低将改变叙利亚仓鼠（Mesocricetus auratus）海马体的主要功能，从记忆形成（通过 LTP、去极化和新的 LTD）转变为增加冬眠期。我们发现，在年轻（<30 天）和成年（>60 天）仓鼠的海马体 CA1 锥体神经元中，低频刺激后的诱发反应减少，这表明在温度>20°C 时，来自幼鼠和成年鼠的海马切片中均产生了新的 LTD。然而，在温度低于 20°C 时，神经集合的同步（LTD 产生的要求）明显恶化，这意味着在冬眠的仓鼠中不能产生新的 LTD。尽管如此，即使在温度低于 16°C 的情况下，锥体神经元仍然可以产生动作电位，这些动作电位可能会穿过神经通路，抑制上行觉醒系统（ARS）。此外，组胺增加了这些锥体细胞的兴奋性。综上所述，这些发现与假设一致，即叙利亚仓鼠的海马体回路在大脑低温下仍能保持运作，并抑制 ARS 以延长发作持续时间，尽管在这些低温下记忆形成受到抑制。
