Wednesday, March 7, 2007

3.7.07

The readings this week focused on an individual’s capacity to remember particular things. When I first began the readings (and particularly, in McGaugh), I wondered how memory had anything to do with emotions. Prior to this, I’ve never really made any concrete connection between the two; they’ve only seemed to be abstract concepts that have somehow indirectly related to each other. After reading chapter five, it made a little bit more sense, but I still feel as though we’re left with the question: How much should we remember? I found the issue of selectivity particularly important; memory is allegedly influenced by the impact of certain events, but what dictates the impact? Norepeniphrine, or an alternate stress hormone? We never really think about what our "brain" chooses to do (or automatically does) when any type of event happens (be it significant or insignificant). What we should and should not know, as far as memory is concerned, still seems to be out of our control; and that might be a good thing. I felt as though this reading brought up one of the key controversies in bioethics right now; that is, is it acceptable to use beta/stress blockers to "downsize" the effects of particular events, and who is capable of judging what events are worthy of this particular type of medication? Our innate biological functions seem to work as a result of some sort of evolutionary process (even though this may not be entirely proven, yet), and one has to wonder why, exactly, the brain chooses particular things to remember (whether it be September 11th, or what was for lunch last Thursday). I still feel like I’m left with no answers, and I still want a solution to the Amygdala-hippocampus debate (if there is one)!

Tuesday, March 6, 2007

March 7 - Memory and Emotion

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?

emotional remembering

All of the readings for this week seemed to focus on the formation and recall of emotional memories. We have examined how basic memories are formed, but these readings focused on particularly intense or traumatic situations. There were moments when I felt like a lot of my questions about memory were being answered in fantastic ways and other moments when I was absolutely confused and didn’t want to be. For example, McGaugh’s section “Nothing like a little stress” (McGaugh, 97) covered a lot about the relationship between norepinephrine, epinephrine and the amygdala. The primary discussion revolved around how the releasing of stress hormones increases the intensity of a memory. There was a lot about the exact process that I would like to know about, but I’m still pretty confused after reading it over several times. I understand the implications of stress hormones on the intensity of memory that he discussed during those few pages, and I’m just lost as to the exact process of how that occurs.

On this same issue, LeDoux points out that slight stress can enhance a memory, due to the release of adrenaline. He attributes this to the increasing activity of the amygdala under stress. On the contrary, the hippocampus falters under stress, which explains memory loss in exceptionally intense situations. He continues his discussion noting, “If indeed the hippocampus is impaired and the amygdala facilitated by stress, it would suggest the possibility that stress shifts us into a mode of operation in which we react to danger rather than think about it.” (LeDoux, 247) This reminded me of last week’s reading, which discussed how when a person is confronted with a threatening situation, their body reacts to the threat before processing what is going on and how to respond to it. I wondered if this fact that “stress shifts us into a mode of operation” would be related to the fact that the amygdala processes innate danger through implicit memory and the hippocampus responds more practically (as in deciding a course of action) as through explicit memory.

The accuracy of our memories was another theme that interested me, as when McGaugh discussed “creative remembering.” (McGaugh, 115) We began addressing this last week in class, through a discussion about how memories can become skewed upon trying to recall them. It is a natural effect, because our new experiences will inevitably affect how we remember old events. I definitely think it’s interesting that the context in which we recall something affects how we think something occurred. It is tempting to think of memories as “imprints” of past experiences and to think that there are certain events that will always stay with you exactly as they occurred. Memory is certainly more deceptive than I realized before beginning all this research.

Monday, March 5, 2007

response for week 8

In chapter five of McGaugh we are presented with a greater articulation of the concept of “flashbulb memory” developed by Roger Brown and James Kulik. Flashbulb memory, as the word “flashbulb” would seem to suggest, is not photographic and does not provide accurate or complete memories necessarily. Flashbulb memory seems to be an umbrella term for strong, semantic memories that stem from an intense emotional experience, one that can be referred to in a more or less concise way. They are vivid and clear in the sense that whatever happened to structure these memories contained intense emotional content. This idea seems to be the most significant in the relationship between memory and emotion throughout our readings for this week because, as most of the data presented in LeDoux, McGaugh and the LaBar and Cabeza article suggests, the process to determine what we remember, how we remember it, and what physically and psychologically happens in the event and the progression following it, is tied to an emotional arousal occurring during or after a significant experience.
I found McGaugh’s study of the use of drugs on this effect to be very interesting and simultaneously confusing. He studied the use of stimulants, adrenalin boosters, and beta-blockers in lab rats to determine if said drugs affected the memory process. What he found was that the stimulants did increase the ability to learn and memorize and that the beta-blockers had the opposite effect. Further in his research, he also found a direct relation to the use of these drugs in the amygdala and the hippocampus supporting his claim that the emotional impact on memory is also significant. McGaugh also suggested that applying this data to humans would prove effective, i.e. giving beta-blockers to patients admitted into the ER after experiencing a traumatic event (like a car crash) might suppress, to some extent, post traumatic stress disorder (PTSD) because the process of remembering would be stifled. While this is an interesting claim, I couldn’t help but think about the previous distinction of memory versus learning/performance. We haven’t yet begun to figure out the complexity of what exactly makes up a memory (in humans or animals) therefore the exaggeration or repression of them (within a specific episode) seems unlikely at this point and time. It seems kind of obvious to me that stress hormones would increase an awareness of an event that would lead to a more detailed memory, but how would this process turn out in a study of long term memory? More significantly, how would this process relate to flashbulb memory in a study where participants had to be administered the drug immediately after experiencing a significantly stressful event? How would you calculate this?
Another point that I found interesting in the readings was McGaugh’s reference to remembering as a “creative act” (p. 115). How we remember and what we remember ties to our creative processes because of our nature, as humans, to be storytellers. This kind of relates to our discussion last week of mnemonics, yet the inherent process to develop stories and believe them as truths is interesting in relation to our discussion of integrated/non-integrated memory. I often find that certain memories I feel that I had were really memories of my sister’s, who, being a great storyteller, would present her experiences in such a vivid way that I would visualize them and interpret them as my own at a very early age. This is similar to Sir Frederic Bartlett’s idea that we sometimes include coherence in our narrative tellings of events in sacrifice of accuracy. It also ties to the study we read about in McGaugh to convince children that they got lost in a supermarket and consequently provide them with a false memory.
Another idea that is not necessarily related to this, but I found interesting seeing that its kind of similar to gestalt psychology, is LaBar and Cabeza’s use of the term “central gist” in describing emotionally arousing experiences. By this I think they mean the general emotional content of a remembered experience as opposed to specific details. I would really like to see this point developed more in understanding how we might fuse emotional memories, or construct details out of a “central gist” as opposed to the actual details in an event.

Reading Response 3/4/07

Our readings last week in LeDoux and McGaugh discussed the processes of memory and underlying biological systems. The readings this week went into greater detail about the role of the amygdala in affectively implicated memory. Drawing on a body of research, LeDoux and McGaugh suggest a model of the amygdala as exerting influence over other brain structures such as the hippocampus and medial temporal lobe to prioritize memories based on their emotional significance. In particular, the authors focus on research using stress hormones which illustrate the amygdala's powerful role in modulating memory consolidation for fearful experiences. I'd also like to address some issues associated with extinction in greater depth.

Stress hormones such as glucocortocoids and epinephrine play a central role in the 'fight or flight' response evoked in conditioned fear learning experiences. Observations that post training injections of stress hormones enhance memory storage suggest that endogenous stress hormones released during fear conditioning are important for the formation of memories and amplify fear responses.

Research on PTSD and repressed memories also indicate that extreme stress may lead to an inability to consciously access memories although an emotional response still exists. The effect of high levels of stress resulting from traumatic emotional events, LeDoux notes, may result in damage to the hippocampus and, consequently, the inability to form explicit memories although the effects of the amygdala's memory consolidation prevail. It is interesting to note, however, that most of the research focusing on effects of stress have only dealt with prolonged exposure to stress instead of isolated traumatic experiences. It is unclear whether a single traumatic event can cause a great enough stress response to impair the hippocampus. Nevertheless, findings strongly suggest that the amygdala's capacity to consolidate experiences into powerful unconscious agents override the organism's ability to control their response.

I would have liked McGaugh, LeDoux, La Bar and Cabeza's explanations of memory extinction to describe the processes of extinction in greater detail (to be fair, LeDoux says he'll come back to it). From what I can gather, extinction is the process of learning to disassociate a stimulus with a conditioned response. In the case of auditory Pavlovian fear conditioning in rats, the animal would learn to associate an auditory cue with a neutral experience instead of a painful one. This idea is interesting for a number of reasons. First, I think it implies that extinction has nothing to do with forgetting a memory, but is actually a unique learning process. Secondly, in order for extinction to occur, the brain must associate the previously learned context with a new context, which is why animals are highly resistant to extinction when hippocampal damage exists. LeDoux mentions that extinction relies on the connections between the medial temporal cortex and amygdala. As the animal learns to consolidate a new context for the stimulus does this require recalling and comparing the memories? What would happen if an aversive emotional response was replaced with a pleasurable one?

And finally, our readings emphasized memories associated with negative emotions, such as fear. Does the amygdala play as influential a role in memory for pleasurable responses? Are memories associated with pain more powerful than pleasurable responses because there is a greater incentive for the survival of the organism? What about sex?

Sunday, March 4, 2007

Reading Response to 3/4/2007

I notice a common thread that runs through all three of the readings for this week. The authors attempt to determine the involvement of certain brain regions and structures on the creation, retention, and retrieval of memory. However, each author uses a different method in their examination of brain regions and structures involved in memory. The paper “Cognitive Neuroscience of Emotional Memory” examines the brain systems involved in forming, keeping, and retrieving memories using emotional arousal. LeDoux uses anxiety disorders to help explain brain systems and their involvement in memory. McGaugh uses drugs to show how activation occurs in certain regions of the brain in memory. Although each author attacks the issue of memory differently, all of them add something new to our limited knowledge of memory and the brain regions involved.

In “Cognitive neuroscience of emotional memory”, LeBar and Cabeza found evidence that “emotional arousal benefits memory in part by facilitating consolidation processes”(LeBar & Cabeza 55). This means that arousal is important in molding and consolidating new memories. Using PET and fMRI studies, the researchers traced the impact of emotion events at various stages of memory. They discovered that specific brain regions are involved in various aspects of memory; from initial formation, to retaining and to retrieving. LeBar and Cabeza found the most important of these structures is the amygdala which is involved in encoding memories, retrieving memories, and fear conditioning.

LeDoux investigates the effects of anxiety on various aspects of memory. He shows how anxiety and stress cause problems in brain structures involved in memory. “Stressful events can cause malfunctions in the hippocampus… the failure to recall an instigating trauma may be due to a stress-induced breakdown in hippocampal memory function”(LeDoux 240). Stress interferes with the hippocampus and blocks the formation of new memories by shriveling up the dendrites involved in memory formation in the hippocampus. In survivors of severe trauma, the person’s hippocampus has permanently shrunken causing significant memory defects. Anxiety inhibits brain structures that contribute to the memory process.

McGaugh investigates what effect drugs have on memory. He states that “drugs are highly useful as tools in determining the involvement and role(s) of different brain regions in memory consolidation” (McGaugh 71). McGaugh tests the effects of strychnine on a rat’s performance in a maze test. After successfully completing the maze test, half of the rats were injected with saline and the other half were injected with strychnine. The saline rats performed the maze test successfully after a three hour delay. The strychnine rats performed the maze test successfully after a nine hour delay. The strychnine enhanced the memory of the rats. McGaugh goes on to test other drugs and their effects on brain structures. McGaugh injects various drugs into the amygdale, hippocampus, and other related brain regions and observes the results. He discovers that the amygdala is crucial in the involvement of consolidating memories. The hippocampus and caudate nucleus selectively affect place learning and cue learning. Norepinephrine actions in the amygdala play an important role in the creation of memories. His discoveries increase our understanding of how certain regions and structures in the brain affect memory formation and function.

All three readings help to shed light on our limited understanding of memory and how it is created, retained, and retrieved. The authors approach the study of memory with different tools and from different perspectives. However, each author makes new discoveries or confirms previous findings about the nature of memory. They share the common goal of broadening the field of memory research.



LaBar, K.S. & Cabeza, R. (2006). Cognitive neuroscience of emotional memory. Nature Neuroscience Reviews, 7, 54-64.

LeDoux, J. (1996). The Emotional Brain. Simon & Schuster: New York. Chapter 8

McGaugh, J.L. (2003). Memory and Emotion. New York: Columbia. Chapter 4