Why do we remember frightening events so well? Fearful situations (link is external) stimulate the brain to activate the sympathetic nervous system and adrenal glands causing the release of stress neurotransmitters and hormones. These chemicals activate the "flight or fight" response which includes an increase in heart rate to facilitate the delivery of blood to working muscles. They also stimulate a brain structure called the amygdala.
As mentioned in my last post, the amygdala is involved with our experience of fear. I described a woman, identified as S.M., who lacked a functioning amygdala and was indiscriminately trusting and friendly. A second individual, identified as B.P., who also lacks a functioning amygdala, was tested for his ability to remember frightening events. In one study (link is external), B.P. and control subjects were presented with a story that contained both emotionally neutral and disturbing events. Like the control subjects, B.P. reacted strongly to the emotionally arousing parts of the story right after it was told. One week after hearing the story, however, control subjects recalled the disturbing parts of the narrative better than the emotionally neutral parts. B.P. remembered the emotionally neutral sections as well as the control subjects, but he demonstrated no enhanced retention of the emotionally arousing parts. One function of the amygdala may be to assign significance to experiences, particularly those that are frightening and life-threatening, and then to enhance the ability of other brain regions to consolidate memories of those events.
The selective nature of our memory makes sense; our very survival may depend upon learning the lessons from life-threatening episodes. However, our ability to selectively remember traumatic episodes can also harm us. Seven percent of the general population suffer from Post-Traumatic Stress Disorder (PTSD). Episodes which produce intense fear can lead to PTSD with effects that may last for a month or persist for a lifetime Situations that remind the individual of the traumatic event or events can trigger excessive release of stress hormones and over-activation of the amygdala which further augments stress hormone release. The result is severe emotional distress - racing thoughts, anger, and hyper-vigilance. When it comes to the most traumatic events in our lives, we walk a fine line between remembering too much and remembering too little.
The amygdala of the mammalian brain has been historically associated with emotional behavior (e.g., Ref. ), and studies conducted over the past several decades have indicated that this structure also modulates the storage of long-term memories (for review, see Ref. ). In particular, the amygdala confers the influence of emotional arousal on learning and memory processes occurring in other brain regions, such as the hippocampus and dorsal striatum [3, 4].
Within the context of a “multiple systems” approach to memory organization, the hippocampus is a critical part of a neural system mediating what are broadly defined as “cognitive” memories involving explicit, declarative information, such as facts and past experiences . Cognitive memory function of the hippocampus also includes acquisition of spatial cognitive maps, i.e., learned mental representations of space which may be used for allocentric navigation . In contrast, the dorsal striatum mediates associations between stimuli and responses and thus encodes memories broadly defined as procedural, stimulus-response (S-R), or habitual (i.e., perseverative responding following devaluation of the reinforcer) . For instance, the dorsolateral striatum (DLS) mediates habitual lever pressing behavior in instrumental learning situations , as well as acquisition and expression of a consistently reinforced egocentric turning response in the plus-maze .
The hippocampus and dorsal striatum differ not only in terms of their anatomical loci and mnemonic functions, but also these brain regions are differentially influenced by parametric factors, including amount of training, reinforcement schedules, and stress/anxiety . As noted above, the emotional modulation of memory systems is mediated by the amygdala, which becomes active during states of emotional arousal and sends glutamatergic projections to other structures to influence the consolidation of memory . The impact of emotional arousal on memory conferred by the amygdala appears to influence hippocampus- and dorsal striatum-dependent memory differently. For instance, high levels of stress or anxiety typically impair learning and memory functions of the hippocampus and enhance learning and memory functions of the dorsolateral striatum [3, 4].
The present chapter provides an updated review of the emotional modulation of multiple memory systems with a focus on the role of the basolateral amygdala. The review begins by describing evidence for the existence of multiple memory systems in the mammalian brain, and this is followed by a review of the influence of stress and anxiety on hippocampus and dorsal striatum-dependent memory processes. Although emotional arousal potentially influences memory formation in several brain regions, we focus on the hippocampus and dorsal striatum. Potential mechanisms through which the amygdala modulates multiple memory systems are also discussed, including the role of memory system interactions, stress hormones, and synaptic plasticity. The relevance of these findings to understanding and treating some human psychopathologies is also considered.
First, let’s look at the role of the amygdala in memory formation. The main job of the amygdala is to regulate emotions, such as fear and aggression ([link]). The amygdala plays a part in how memories are stored because storage is influenced by stress hormones. For example, one researcher experimented with rats and the fear response (Josselyn, 2010). Using Pavlovian conditioning, a neutral tone was paired with a foot shock to the rats. This produced a fear memory in the rats. After being conditioned, each time they heard the tone, they would freeze (a defense response in rats), indicating a memory for the impending shock. Then the researchers induced cell death in neurons in the lateral amygdala, which is the specific area of the brain responsible for fear memories. They found the fear memory faded (became extinct). Because of its role in processing emotional information, the amygdala is also involved in memory consolidation: the process of transferring new learning into long-term memory. The amygdala seems to facilitate encoding memories at a deeper level when the event is emotionally arousing.