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情緒如何增強記憶

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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.

情緒如何增強記憶
James L. McGaugh, Ph.D.,California大學心理學研究教授、學習與記憶神經生物學中心創建人和中心主任

從對人和對動物的研究中我們知道,一類稱為苯二氮雜平類(benzodiazepine)的減輕憂慮的藥物(例如安定和Halcion)會損傷記憶的鞏固。其它類型的藥物則具有相反的作用,能夠增強記憶,但在學習后的記憶增強發生時馬上用藥才有效。如果在訓練后超過六個小時用藥,那么記憶不會被增強。

這兩類藥物都對杏仁核側底核中的相同受體起作用,這些抑制性神經遞質GABA(伽瑪氨基丁酸)的受體阻止接受神經元的興奮或節制其興奮強度。導致健忘癥的藥物為GABA促效劑(agonists):它們的作用像GABA自身一樣激活GABA受體。增強記憶的藥物則為GABA拮抗劑(antagonists):它們阻止GABA受體的激活。

當我們感到有壓力時所釋放的荷爾蒙也會增強記憶。這就解釋了為什么情緒喚醒對我們回憶事情具有強有力的影響。當大腦意識到危險時, “戰斗還是逃避”的瞬間反應涉及到視丘下部,沿交感神經系統將信號送至腎上腺,尤其是腎上腺髓質,分泌出荷爾蒙腎上腺素(或稱腎上腺素)和降腎上腺素進入血流。腎上腺素使心率加快,降腎上腺素使血壓上升。

如果這個威脅超過幾秒鐘,那么HPA(視丘下部-腦垂體-腎上腺)樞紐將激活。視丘下部釋放出一種稱為CRH(促腎上腺皮質釋放荷爾蒙)的荷爾蒙,刺激腦垂體分泌出ACTH(促腎上腺皮質荷爾蒙),ACTH又刺激腎上腺外部即腎上腺皮質,產生出皮質醇(cortisol)。而皮質醇提升血糖以為戰斗和/或逃跑提供更多的能量。在通過調節杏仁核側底核中的降腎上腺素的釋放來調節記憶力的過程中,腎上腺素和皮質醇都扮演著重要的角色。

即使杏仁核對于情緒性記憶的鞏固極為重要,它并不是存貯長期記憶的部位。動物研究表明,在對一些動物用軟性足部刺激(一種足以引起應激反應的負面體驗)進行訓練,然后通過注射利多卡因使其杏仁核不活動,這些動物仍可以完成訓練任務,它們的記憶未受影響。

我們從對人的實驗了解到,記憶強度由體驗的意義所調節。這種調節涉及了應激荷爾蒙的釋放。在一個實驗中,對兩組受檢者讀一段故事和放映一組幻燈片。他們都看同一組幻燈片,但聽的是兩個不同的故事。一個故事平淡而中和,另一個故事相類似,只是在中間部分有一段激起情感的描述。

兩周后,請這些受檢者敘述他們對那組幻燈片的回憶。聽中性故事的那組能夠同樣或好或壞地回憶起所有故事情節,對幻燈片的回憶從頭到尾沒有區別。但是另一組則對中間部分有更強的記憶,他們在看這部分的時候曾聽過激起情感的描述。

在其后的一個實驗中,實驗開始前給一半的受檢者貝塔阻斷劑(以阻斷腎上腺素作用)。對于那些聽了中性故事的人,貝塔阻斷劑沒有造成他們對幻燈片回憶的差別。但對于那些聽了感人故事的人,貝塔阻斷劑則完全阻斷了他們記憶中激情印象,從而防止對此的記憶變強。

對于被受那些對創傷的清晰記憶所折磨和遭受傷后應激紊亂的人,這些結果具有清楚的提示。可以采用人工的即藥物的方式阻斷傷后應激紊亂的發展,阻斷大腦中應激荷爾蒙的作用。如果我們能夠減小對一次傷害或事故記憶的情緒負擔,那么就能夠減小長期的焦慮。

當情緒與記憶之間的連接正常,結果十分令人滿意:我們記住我們想要記住的重要的和好的事情。如果該系統工作過度,我們會記憶太多或太強烈,從而結果就會減弱。

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