PLoS One：氙气可以删除大脑部分记忆

导读	据《每日科学》网站报道，麦克莱恩医院研究人员报道最新的科研成果表明，氙气或有可能治疗创伤后应激障碍（PTSD）和其他疾病，而此前，氙气被广泛应用于麻醉和诊断成像。相关研究发表在最新一期《公共科学图书馆·综合》(PLoS One)杂志上。

据《每日科学》网站报道，麦克莱恩医院研究人员报道最新的科研成果表明，氙气或有可能治疗创伤后应激障碍（PTSD）和其他疾病，而此前，氙气被广泛应用于麻醉和诊断成像。

哈佛医学院精神病学助理教授、麦克莱恩医院助理心理学家爱德华·G·海洛尼（Edward G. Meloni）表示：“在研究中，我们发现氙气有减少创伤性事件记忆的能力。这是一个激动人心的突破，因为这有可能成为一种新的治疗创伤后应激障碍的疗法。”

这项研究发表在最新一期《公共科学图书馆·综合》(PLoS One)中。梅洛尼和麦克莱恩医院转化成像实验室主管马克·J·考夫曼（Marc J. Kaufman）博士一起研究了低浓度氙气是否会干扰“重新整合（reconsolidation）”过程——重新激活记忆，变得容易修改。梅洛尼解释道：”从之前的研究中我们知道，每一次情感回忆被唤起时，大脑实际上会把它当做新记忆进行恢复。根据这些情况，我们决定是否测试，是否可以在恐惧记忆被再次激活后，通过立即引入氙气，从而调整该过程。“

研究人员利用了一种恐惧状态下的PTSD动物模型，训练老鼠害怕环境因素，同时配以简单的足底电击。然后，老鼠被再次放置在相同的环境因素中，以唤醒恐惧记忆，测量它们的冰冻反馈来度量恐惧程度。

梅洛尼博士提到：“我们发现，暴露在氙气中可以阻断NMDA受体参与大脑记忆形成，最高可显着减少两周的记忆，就好像害怕的动物不再记得这些。”

梅洛尼指出，氙气一类气体的固有属性是比较理想治疗素材。因为氙气可以快速进出大脑，准确介入大脑唤起回忆的时间，并能够精确控制用量。

参考文献

Xenon Impairs Reconsolidation of Fear Memories in a Rat Model of Post-Traumatic Stress Disorder (PTSD)

文献检索：DOI: 10.1371/journal.pone.0106189

Xenon (Xe) is a noble gas that has been developed for use in people as an inhalational anesthestic and a diagnostic imaging agent. Xe inhibits glutamatergic N-methyl-D-aspartate (NMDA) receptors involved in learning and memory and can affect synaptic plasticity in the amygdala and hippocampus, two brain areas known to play a role in fear conditioning models of post-traumatic stress disorder (PTSD). Because glutamate receptors also have been shown to play a role in fear memory reconsolidation – a state in which recalled memories become susceptible to modification – we examined whether Xe administered after fear memory reactivation could affect subsequent expression of fear-like behavior (freezing) in rats. Male Sprague-Dawley rats were trained for contextual and cued fear conditioning and the effects of inhaled Xe (25%, 1 hr) on fear memory reconsolidation were tested using conditioned freezing measured days or weeks after reactivation/Xe administration. Xe administration immediately after fear memory reactivation significantly reduced conditioned freezing when tested 48 h, 96 h or 18 d after reactivation/Xe administration. Xe did not affect freezing when treatment was delayed until 2 h after reactivation or when administered in the absence of fear memory reactivation. These data suggest that Xe substantially and persistently inhibits memory reconsolidation in a reactivation and time-dependent manner, that it could be used as a new research tool to characterize reconsolidation and other memory processes, and that it could be developed to treat people with PTSD and other disorders related to emotional memory.