Saito Shinichi, Kimura Satoshi, Adachi Naoki, Numakawa Tadahiro, Ogura Akihiko, Tominaga-Yoshino Keiko
Laboratory of Synaptic Plasticity, Osaka University Graduate School of Frontier Biosciences, Suita, Osaka 565-0871 Japan.
National Center of Neurology and Psychiatry, Kodaira 187-8551 Tokyo, Japan.
Sci Rep. 2016 Jan 14;6:19287. doi: 10.1038/srep19287.
Previously, in organotypic slice culture of rodent hippocampus we found that three repeated inductions of LTP, but not a single induction, led to a slow-developing long-lasting enhancement of synaptic strength coupled with synapse formation. Naming this structural plasticity RISE (repetitive LTP-induced synaptic enhancement) and assuming it to be a potential in vitro reproduction of repetition-dependent memory consolidation, we are analyzing its cellular mechanisms. Here, we applied a glucocorticoid to the culture to mimic acute excess stress and demonstrated its blockade of RISE. Since excess stress interferes with behavioral memory consolidation, the parallelism between RISE in vitro and memory consolidation in vivo is supported. We recently reported that RISE developed after stochastic processes. Here we found that the glucocorticoid interfered with RISE by suppressing the increment of dendritic spine fluctuation that precedes a net increase in spine density. The present study provides clues for understanding the mechanism of stress-induced memory defects.
此前，在啮齿动物海马体的器官型切片培养中，我们发现三次重复诱导长时程增强（LTP），而非单次诱导，会导致突触强度缓慢发展的长期增强，并伴有突触形成。我们将这种结构可塑性命名为RISE（重复性LTP诱导的突触增强），并假定它是依赖重复的记忆巩固的一种潜在体外再现形式，我们正在分析其细胞机制。在此，我们向培养物中应用糖皮质激素以模拟急性应激，并证明其对RISE的阻断作用。由于过度应激会干扰行为记忆巩固，因此支持了体外RISE与体内记忆巩固之间的平行关系。我们最近报道RISE是在随机过程之后发展起来的。在这里，我们发现糖皮质激素通过抑制在脊柱密度净增加之前的树突棘波动的增加来干扰RISE。本研究为理解应激诱导的记忆缺陷机制提供了线索。
