A common theme of this week’s readings is stress and its relation to emotion and memory. McGaugh reviews the evidence that memory consolidation can be enhanced or inhibited with drugs over a wide variety of memory tasks. For such improvement or determent to occur, the drugs must be administered soon after the task, as it has been shown that memory consolidation takes place only a short period of time after something is learned. Whether through direct or indirect action on the amygdala, memory consolidation is enhanced by stimulation and hindered by inhibition. For instance, electrical stimulation of the amygdala after training in a task improves memory. Norepinephrine release in the amygdala is also an important aid in memory consolidation. Norepinephrine levels can be increased through the differing actions of the stress hormones epinephrine and cortisol. The release of these and many other stimulating hormones and neurotransmitters can be pharmacologically induced, with the effect of aiding memory consolidation. On the other hand, if norepinephrine is inhibited by drug administration, the opposite effect (consolidation hindrance) will occur.
Artificially induced stress is not the only kind that acts on the amygdala to enhance memory. It has been shown that people have stronger and more accurate memories of emotionally arousing words, movies, and general experiences. Still, that even the most emotional and frequently revisited memories are not 100% accurate is a point that repeatedly appears in the literature. Elizabeth Loftus’s work, highlighting the realities of false memories such as being lost in a mall and being sexually abused by a baby-eating, animal-loving cult member, is a testament to this.
Stress does not always have a positive effect on memory. The failed synthesis of cortisol (?) can result in the temporary blocking of well-learned information, as in the case of a fully prepared actor forgetting his lines. In addition, prolonged levels or a single event of high stress can override the hippocampus’s attempts to keep the stress in check, thereby compromising its normal function in explicit memory. It is also possible that the memory failure is partially due to the fact that stress interferes with long-term potentiation in the hippocampus. Autopsies of monkeys living under the ever-present stress of a dominant male revealed that the structure was visibly degenerated. The impairment of the hippocampus along with an unaffected amygdala would explain why a victim might not explicitly recollect a particularly traumatic event, but still fall privy to the devastating emotions that are associated. This evidence does not put Freud’s theory of repression in a good light. LeDoux once again successfully points evolutionary importance: the amygdala is facilitated by stress and the hippocampus impaired by it so that we can react to danger rather than think about it.
Arousal of the amygdala does improve memory, but at significant costs. I substitute "arousal" for "stress" here because emotional experiences need not be "stressful," per say, to be firmly established in memory; LaBar and Cabeza note that amygdala activation during encoding correlates positively with delayed recall accuracy for emotionally arousing pictures that are both attractive and aversive. Nevertheless, it is tempting to conclude that traumatic memories are the ones that have the most powerful effect on memory. Whether taken from a psychoanalytic or behavioral stance, anxiety is the result of traumatic learning experiences. Anxiety disorders like phobias, panic, PTSD, and OCD are fairly common problems that are all related to fear conditioning, and they have no easy solution. LeDoux proposes a few possibilities as to why these conditions are particularly resistant to extinction in humans: abnormal functioning of the medial prefrontal cortex, which also may be due to stress; evolutionary "preparedness" to fear things that were dangerous to our ancestors; and, perhaps most interestingly, "cell assemblies" of spontaneously firing neurons that result from Hebbian learning (conditioning), which, again, may be strengthened merely with stress.
A few questions I have about the readings:
-To what extent is the medial prefrontal cortex different in people with anxiety disorders? In addition to its mediation of extinction, the PFC is involved in decision making and higher thinking. Are there any drugs that improve this structure’s performance?
-What is known about the learning/performance distinction that McGaugh avoids talking about? Damasio’s patient Elliot, who had PFC damage, seemed to lack behavioral but not cognitive knowledge.
-McGaugh notes that it is unlikely that animals explicitly rehearse training experience. But don’t their hippocampal abilities indicate that they can?
-Labar & Cabeza article differentiates between encoding and consolidation. What is the difference between the two?
-I’m sure it differs on an individual basis, but are there any neural markers that predict stress-induced hipoocampal failure?
Subscribe to:
Post Comments (Atom)
3 comments:
Like Matt, I was also interested in the effects of
anxiety and stress on memory. I was curious as to thebrain functions that take place after and an extremely traumatic event or a highly stressful event. In last week’s reading we touched on a woman driving her car as it skidded over ice. After such an event, how would a high level of anxiety effect memory consolidation? And, on the issue of repression, inactivation verse activation, is there a correlation between anxiety and repression? When does the brain choose to forget, and when does it choose to remember?
Post a Comment