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情绪如何增强记忆

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How Emotions Strengthen Memory
James L. McGaugh, Ph.D.,California

From both human and animal studies, we know that a certain class of anxiety-reducing drugs called benzodiazepines (Valium and Halcion, for example) impair memory consolidation. Other classes of drugs have the opposite effect and can enhance memory, but only if they are administered shortly after learning, when memory consolidation is occurring. If the injections occur more than six hours after training, memory is not enhanced.

Both kinds of drugs work on the same receptors in the basolateral nucleus of the amygdala, receptors for the inhibitory neurotransmitter GABA, which blocks the firing of the receiving neuron or moderates the strength of its firing. The amnesia-inducing drugs are GABA agonists: they act like GABA itself to activate the GABA receptors. The memory enhancing drugs are GABA antagonists: they block activation of the GABA receptors.

Memory also is enhanced by hormones that are released when we experience stress. This explains why emotional arousal has such a powerful influence on how well we remember things. When the brain senses danger, the instant fight-or-flight response involves the hypothalamus sending signals along the sympathetic nervous system to the adrenal glands, specifically to the adrenal medulla, which secrete the hormones epinephrine (also called adrenaline) and norepinephrine into the blood stream. Adrenaline raises the heart rate; norepinephrine raises blood pressure.

If the threat continues for more than a few seconds, the HPA (hypothalamus-pituitary-adrenal) axis is activated. The hypothalamus releases a hormone called CRH (corticotropin releasing hormone), which stimulates the pituitary gland to secrete ACTH (adrenocorticotropic hormone), which in turn stimulates the outer part of the adrenal glands, the adrenal cortex, to produce cortisol. Cortisol, among other things, increases the supply of blood glucose to make more energy available, enabling the fight and/or the flight. Both epinephrine and cortisol play a very powerful role in regulating the strength of memory by regulating the release of norepinephrine in the basolateral nucleus of the amygdala.

Even though the amygdala is crucial to the consolidation of emotional memories, it is not the site of long-term storage of the memories. Animal studies show that when animals are trained with mild foot shocks (a sufficiently negative experience to induce the stress response) and then have their amygdalas inactivated by injections of lidocaine, they can still perform the training task; their memory is not affected.

We know from human experiments that the strength of a memory is regulated by the significance of the experience. The regulation involves the release of stress hormones. In one experiment, two groups of subjects were read a story and shown a series of slides. They all saw the same slides, but they heard two different stories. One story was flat and neutral; the other story matched it except for an emotionally arousing description in the middle.

Two weeks later, the subjects were asked to state what they remembered of the slides. The group that heard the neutral story remembered the slides from all parts of the story equally well (or poorly); there was no difference in recall of the slides from the beginning, middle, or end of the story. The other group, however, had significantly enhanced recall of the slides in the middle, the ones they were looking at when they heard the emotionally arousing description.

In a subsequent experiment, half the subjects were given a beta blocker (to block epinephrine effects) before the experiment started. For those who heard the neutral story, the beta blocker made no difference in their recall of the slides. But in those who heard the emotional story, the beta blocker completely blocked the arousing effect of emotion on memory, preventing the memory from becoming strong.

These results have clear implications for people who are plagued by vivid memories of a trauma and are suffering from post-traumatic stress disorder. It may be possible to block the development of post-traumatic stress disorder by artificially--that is, pharmaceutically--blocking the effects of stress hormones in the brain. If we can reduce the emotional charge of the memory of an assault or an accident, we can reduce the long-term anxiety.

When the connection between emotion and memory works well, the results are very satisfying: we remember the important and good things that we want and need to remember. When the system is overworked, we may remember too much, or too intensely, and the result may be debilitating.

情绪如何增强记忆
James L. McGaugh, Ph.D.,California大学心理学研究教授、学习与记忆神经生物学中心创建人和中心主任

从对人和对动物的研究中我们知道,一类称为苯二氮杂平类(benzodiazepine)的减轻忧虑的药物(例如安定和Halcion)会损伤记忆的巩固。其它类型的药物则具有相反的作用,能够增强记忆,但在学习后的记忆增强发生时马上用药才有效。如果在训练后超过六个小时用药,那么记忆不会被增强。

这两类药物都对杏仁核侧底核中的相同受体起作用,这些抑制性神经递质GABA(伽玛氨基丁酸)的受体阻止接受神经元的兴奋或节制其兴奋强度。导致健忘症的药物为GABA促效剂(agonists):它们的作用像GABA自身一样激活GABA受体。增强记忆的药物则为GABA拮抗剂(antagonists):它们阻止GABA受体的激活。

当我们感到有压力时所释放的荷尔蒙也会增强记忆。这就解释了为什么情绪唤醒对我们回忆事情具有强有力的影响。当大脑意识到危险时, “战斗还是逃避”的瞬间反应涉及到视丘下部,沿交感神经系统将信号送至肾上腺,尤其是肾上腺髓质,分泌出荷尔蒙肾上腺素(或称肾上腺素)和降肾上腺素进入血流。肾上腺素使心率加快,降肾上腺素使血压上升。

如果这个威胁超过几秒钟,那么HPA(视丘下部-脑垂体-肾上腺)枢纽将激活。视丘下部释放出一种称为CRH(促肾上腺皮质释放荷尔蒙)的荷尔蒙,刺激脑垂体分泌出ACTH(促肾上腺皮质荷尔蒙),ACTH又刺激肾上腺外部即肾上腺皮质,产生出皮质醇(cortisol)。而皮质醇提升血糖以为战斗和/或逃跑提供更多的能量。在通过调节杏仁核侧底核中的降肾上腺素的释放来调节记忆力的过程中,肾上腺素和皮质醇都扮演着重要的角色。

即使杏仁核对于情绪性记忆的巩固极为重要,它并不是存贮长期记忆的部位。动物研究表明,在对一些动物用软性足部刺激(一种足以引起应激反应的负面体验)进行训练,然后通过注射利多卡因使其杏仁核不活动,这些动物仍可以完成训练任务,它们的记忆未受影响。

我们从对人的实验了解到,记忆强度由体验的意义所调节。这种调节涉及了应激荷尔蒙的释放。在一个实验中,对两组受检者读一段故事和放映一组幻灯片。他们都看同一组幻灯片,但听的是两个不同的故事。一个故事平淡而中和,另一个故事相类似,只是在中间部分有一段激起情感的描述。

两周后,请这些受检者叙述他们对那组幻灯片的回忆。听中性故事的那组能够同样或好或坏地回忆起所有故事情节,对幻灯片的回忆从头到尾没有区别。但是另一组则对中间部分有更强的记忆,他们在看这部分的时候曾听过激起情感的描述。

在其后的一个实验中,实验开始前给一半的受检者贝塔阻断剂(以阻断肾上腺素作用)。对于那些听了中性故事的人,贝塔阻断剂没有造成他们对幻灯片回忆的差别。但对于那些听了感人故事的人,贝塔阻断剂则完全阻断了他们记忆中激情印象,从而防止对此的记忆变强。

对于被受那些对创伤的清晰记忆所折磨和遭受伤后应激紊乱的人,这些结果具有清楚的提示。可以采用人工的即药物的方式阻断伤后应激紊乱的发展,阻断大脑中应激荷尔蒙的作用。如果我们能够减小对一次伤害或事故记忆的情绪负担,那么就能够减小长期的焦虑。

当情绪与记忆之间的连接正常,结果十分令人满意:我们记住我们想要记住的重要的和好的事情。如果该系统工作过度,我们会记忆太多或太强烈,从而结果就会减弱。

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