THE AMYGDALA

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.

THE HIPPOCAMPUS

Another group of researchers also experimented with rats to learn how the hippocampus functions in memory processing ([link]). They created lesions in the hippocampi of the rats, and found that the rats demonstrated memory impairment on various tasks, such as object recognition and maze running. They concluded that the hippocampus is involved in memory, specifically normal recognition memory as well as spatial memory (when the memory tasks are like recall tests) (Clark, Zola, & Squire, 2000). Another job of the hippocampus is to project information to cortical regions that give memories meaning and connect them with other connected memories. It also plays a part in memory consolidation: the process of transferring new learning into long-term memory.

Injury to this area leaves us unable to process new declarative memories. One famous patient, known for years only as H. M., had both his left and right temporal lobes (hippocampi) removed in an attempt to help control the seizures he had been suffering from for years (Corkin, Amaral, González, Johnson, & Hyman, 1997). As a result, his declarative memory was significantly affected, and he could not form new semantic knowledge. He lost the ability to form new memories, yet he could still remember information and events that had occurred prior to the surgery.

THE CEREBELLUM AND PREFRONTAL CORTEX

Although the hippocampus seems to be more of a processing area for explicit memories, you could still lose it and be able to create implicit memories (procedural memory, motor learning, and classical conditioning), thanks to your cerebellum ([link]). For example, one classical conditioning experiment is to accustom subjects to blink when they are given a puff of air. When researchers damaged the cerebellums of rabbits, they discovered that the rabbits were not able to learn the conditioned eye-blink response (Steinmetz, 1999; Green & Woodruff-Pak, 2000).

Other researchers have used brain scans, including positron emission tomography (PET) scans, to learn how people process and retain information. From these studies, it seems the prefrontal cortex is involved. In one study, participants had to complete two different tasks: either looking for the letter a in words (considered a perceptual task) or categorizing a noun as either living or non-living (considered a semantic task) (Kapur et al., 1994). Participants were then asked which words they had previously seen. Recall was much better for the semantic task than for the perceptual task. According to PET scans, there was much more activation in the left inferior prefrontal cortex in the semantic task. In another study, encoding was associated with left frontal activity, while retrieval of information was associated with the right frontal region (Craik et al., 1999).

NEUROTRANSMITTERS

There also appear to be specific neurotransmitters involved with the process of memory, such as epinephrine, dopamine, serotonin, glutamate, and acetylcholine (Myhrer, 2003). There continues to be discussion and debate among researchers as to which neurotransmitter plays which specific role (Blockland, 1996). Although we don’t yet know which role each neurotransmitter plays in memory, we do know that communication among neurons via neurotransmitters is critical for developing new memories. Repeated activity by neurons leads to increased neurotransmitters in the synapses and more efficient and more synaptic connections. This is how memory consolidation occurs.

It is also believed that strong emotions trigger the formation of strong memories, and weaker emotional experiences form weaker memories; this is called arousal theory (Christianson, 1992). For example, strong emotional experiences can trigger the release of neurotransmitters, as well as hormones, which strengthen memory; therefore, our memory for an emotional event is usually better than our memory for a non-emotional event. When humans and animals are stressed, the brain secretes more of the neurotransmitter glutamate, which helps them remember the stressful event (McGaugh, 2003). This is clearly evidenced by what is known as the flashbulb memory phenomenon.

A flashbulb memory is an exceptionally clear recollection of an important event ([link]). Where were you when you first heard about the 9/11 terrorist attacks? Most likely you can remember where you were and what you were doing. In fact, a Pew Research Center (2011) survey found that for those Americans who were age 8 or older at the time of the event, 97% can recall the moment they learned of this event, even a decade after it happened.

Most people can remember where they were when they first heard about the 9/11 terrorist attacks. This is an example of a flashbulb memory: a record of an atypical and unusual event that has very strong emotional associations. (credit: Michael Foran)