By the end of this section, you will be able to:
- Explain the brain functions involved in memory
- Recognize the roles of the hippocampus, amygdala, and cerebellum
Are memories stored in just one part of the brain, or are they stored in many different parts of the brain? Karl Lashley began exploring this problem, about 100 years ago, by making lesions in the brains of animals such as rats and monkeys. He was searching for evidence of the engram: the group of neurons that serve as the “physical representation of memory” (Josselyn, 2010). First, Lashley (1950) trained rats to find their way through a maze. Then, he used the tools available at the time—in this case a soldering iron—to create lesions in the rats’ brains, specifically in the cerebral cortex. He did this because he was trying to erase the engram, or the original memory trace that the rats had of the maze.
Lashley did not find evidence of the engram, and the rats were still able to find their way through the maze, regardless of the size or location of the lesion. Based on his creation of lesions and the animals’ reaction, he formulated the equipotentiality hypothesis: if part of one area of the brain involved in memory is damaged, another part of the same area can take over that memory function (Lashley, 1950). Although Lashley’s early work did not confirm the existence of the engram, modern psychologists are making progress locating it.
Many scientists believe that the entire brain is involved with memory. However, since Lashley’s research, other scientists have been able to look more closely at the brain and memory. They have argued that memory is located in specific parts of the brain, and specific neurons can be recognized for their involvement in forming memories. The main parts of the brain involved with memory are the amygdala, the hippocampus, the cerebellum, and the prefrontal cortex.
Figure 8.07. The amygdala is involved in fear and fear memories. The hippocampus is associated with declarative and episodic memory as well as recognition memory. The cerebellum plays a role in processing procedural memories, such as how to play the piano. The prefrontal cortex appears to be involved in remembering semantic tasks.
Long term memory represents the final stage in the information-processing model where informative knowledge is stored permanently (the idea of memory permanences will be discussed in a later section). Memories we have conscious storage and access to are known as explicit memory (also known as declarative memory) and are encoded by the hippocampus, the entorhinal cortex, and the perihinal cortex which are important structures in the limbic system. The limbic system represents a set of brain structures located on both sides of the thalamus, immediately beneath the cerebral cortex, and is important for a variety of functions including emotion, motivation, long-term memory, and olfaction.
Within the category of explicit memories, episodic memories represent times, places, associated emotions and other contextual information that make up autobiographical events. These types of memories are sequences of experiences and past memories that allows the individual to figuratively travel back in time to relive or recall the event that took place at a particular time and place. Episodic memories have been demonstrated to rely heavily on neural structures that were activated during a procedure when the event was being experienced. Gottfried and colleagues (2004) used fMRI scanners to observe brain activity when participants were trying to remember images they had first viewed in the presence of a specific scent. When recalling the images participants had viewed with the accompanying smell, areas of the primary olfactory cortex (the prirform cortex) were more active compared to no scent pairing conditions (Gottfried, Smith, Rugg & Doland, 2004), suggesting memories are retrieved by reactivating the sensors areas that were active while experiencing the original event. This indicates sensory input is extremely important for episodic memories which we use to try to recreate the experience of what had occurred.
Semantic memory represents a second of the three main types of explicit memory and refers to general world knowledge we possess and have collected throughout our lives. These facts about the world, ideas, meanings and concepts are mixed with our experiences from episodic memory and are emphasized by cultural differences. Within the field of cognitive neuroscience there are many views regarding the locations in the brain where semantic memories are stored. One view suggests that semantic memories are stored by the same neural structures that assist in creating episodic memories. Areas such as the medial temporal lobes, the hippocampus and fornix which encode the information and build connections with areas of the cortex where they can be accessed at a later time. Other research has suggested that the hippocampus and neighboring structures of the limbic system are more crucial to the storage and retrieval of semantic memories than areas related to motor activities or sensory processing used during the time of encoding (Vargha-Khadem et al., 1997). Still other groups have suggested semantic memories are retrieved from areas of the frontal cortex and stored in areas of the temporal lobe (Hartley et al., 2014, Binder et al., 2009) . Overall, evidence suggests that many areas of the brain are related to the storage and retrieval of explicit memory as opposed to singular structures.
The final main group of memory under the category of explicit memory is known as Autobiographical memory. This memory system is made up of both episodic, and semantic aspects of memory and is a collection of memories specifically related to the self. This could be how you look, your height, specific meaningful points in your life, or the general idea of your concept of self. The specific locations where this type of memory are stored and accessed are especially controversial due to the close relationship between autobiographical information and conscious experience. Conway and Pleydell-Pearce (2000) suggested a model describing autobiographical memories as transitory mental compositions stored within a self-memory system containing an autobiographical knowledge base and current goals of the working self. According to this approach, within the self memory system, control processes exist that modulate the ability to associate information to the self knowledge base by continually editing cues used to activate autobiographical memory. Therefore the concepts of self and memories related to self can be influenced by the context of self perceptions at the time of memory encoding. Modern neuroimaging research suggests that autobiographical memory is distributed throughout many complex neural networks including the recruitment neuron groups in the medial and ventrolateral prefrontal cortex, as well as the medial and lateral temporal cortex, the temporal-parietal junction, posterior cingulate cortex, and the cerebellum (Svoboda, E., McKinnon, M. C., Levine, B., 2006).
In contrast to the memory systems covered above related to explicit encoding and retrieval memory processes, implicit memory as discussed in the previous section refers to memories that are acquired and recalled unconsciously. Modern research has suggested that the cerebellum, the basal ganglia (a group of subcortical structures associated with voluntary motor control, procedural learning, and emotion as well as many other behaviors), the motor cortex, and various areas of the cerebral cortex (Dharani, 2014) are related to the storage and retrieval of implicit memory.
The amygdala is an extremely important structure for the creation and recall of both explicit and implicit memory. The main job of the amygdala is to regulate emotions, such as fear and aggression. The amygdala plays a part in how memories are stored as information storage is influenced by emotions and stress. Jocelyn (2010) paired a neutral tone with a foot shock to a group of rats to evaluate the rats fear related to the conditioning with the tone. This produced a fear memory in the rats. After being conditioned, each time the rats 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 in rats. They found the fear memory became extinct (the fear memory faded). 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. For instance, in terms of the Craik and Lockhart’s (1972) depth of processing model, recent research has demonstrated memories encoded of images that elicit an emotional reaction tend to be remembered more accurately and easier compared to neutral images (Xu et al., 2014). Additionally, fMRI research has demonstrated stronger coupled activation of the amygdala and hippocampus while encoding predicts stronger and more accurate recall memory ability (Phelps, 2004). Greater activation of the amygdala predicting higher probabilities of accurate recall provides evidence illustrating how association with an emotional response can create a deeper level of processing during encoding, resulting in a stronger memory trace for later recall.
The hippocampal formation is made up of a group of substructures including the hippocampus, the dentate gyrus, and the subiculum all of which are located in the interior of the temporal lobe organized in a similar shape to a letter C. Together these structures represent the main areas of the brain associated with the formation of long term memories.
Clark, Zola and Squire (2000) experimented with rats to learn how the hippocampus functions in memory processing. 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 creating memories, specifically normal recognition memory as well as spatial memory (when the memory tasks are like recall tests). The hippocampus also projects information to cortical regions that give memories meaning and connect them to other bits of information. In addition, it also plays a main role in memory consolidation: the process of transferring new learning into long-term memory.
Injury to this area interferes with the ability to form new memories but does not significantly impair their ability to retrieve memories already stored as long term memories (Hudspeth et al., 2013). 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 (explicit) 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. His story provides strong evidence in humans that the hippocampus is mainly related to memory consolidation.
THE CEREBELLUM AND PREFRONTAL CORTEX
The cerebellum plays a large role in implicit memories (procedural memory, motor learning, and classical conditioning). For example, an individual with damage to their hippocampus will still demonstrate a conditioning response to blink when they are given a series of puffs of air to their eyes. However, 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). This experiment demonstrates the important role the cerebellum plays in the formation of implicit memories and conditioned responses.
Recent estimates of counts of neurons in various brain regions suggests there are about 21 to 26 billion neurons in the human cerebral cortex (Pelvig et al., 2008), and 101 billion neurons in the cerebellum (Andersen, Korbo & Pakkenberg, 1992), yet the cerebellum makes up roughly only 10% of the brain (Siegelbaum et al., 2013). The cerebellum is composed of a variety of different regions that receive projections from different parts of the brain and spinal cord, and project mainly to motor related brain systems in the frontal and parietal lobes.
In addition to contributions to implicit memory, conditioned responses, fine motor movements, posture and coordination, the cerebellum also maintains internal representations of the external world, which allow you to navigate through your living room to find your keys in complete darkness, and professional baseball players to coordinate their movement so they can catch outfield fly balls.
Other researchers have used brain imaging measuring metabolic processes, including positron emission tomography (PET) scans, to learn how people process and retain information. From these studies, the prefrontal cortex appears to be active during a variety of memory related tasks. 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, and reported much better recall for the semantic task compared to 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).
Another widely held view of prefrontal cortex function is that it encodes task relevant information in working memory (Baddeley, 2003). Many studies have shown greater amounts of prefrontal cortex activity during delay periods in working memory tasks demonstrating prefrontal rehearsal processes leading to the transition of information from short term working memory to long term memory (Wilson et al., 1993; Levy & Goldman-Rakic, 2000). More recent work evaluating greater prefrontal activity during working memory task delays suggest the activity of the prefrontal cortex during these delay periods may not be neural signatures of long term memory encoding, but may actually be top-down signals that influence encoding in posterior sensory and association areas where the actual working memory representations are maintained (Lara & Wallis, 2015).
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 the specific roles each neurotransmitter plays (Blockland, 1996). Although there is much debate defining conclusive causal relationships between specific neurotransmitters and specific behaviors by way of experimental design, researchers are able to use two general methods to make inferences about these relationships.
The first method is known as an interventional strategy pharmacological tools or lesions/stimulation are used on specific neurotransmitters and their receptors. The second method is known as a correlational method, where different naturally occurring conditions (neurological diseases, aging) that affect different neurotransmitter systems are compared in humans or animal models. Using these methods, several neurotransmitter groups and pathways have been consistently found to be important for a variety of memory processes (Chapoutier, 1989; Decker and McGaugh, 1991). Repeated activity by neurons leads to greater releases of neurotransmitters in the synapses and stronger neural connections between neuron groups creating memory consolidation.
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 to remember the stressful event (Szapiro et al, 2003). This provides the functional basis of a phenomenon commonly referred to as flashbulb memory.
Early research into functional properties of glutamate used a compound known as proline to study responses in the avian (bird) retina. Cherkin, Eckardt and Gerbrandt (1976), found the administration of proline would reduce learning and memory in birds, suggesting that because proline acts as a glutamate antagonist (reducing the release of glutamate in the synapse), glutamate must be involved in some process related to learning and memory. Further studies used other glutamate antagonists to demonstrate that overall, reducing the amount of glutamate in the synapse reduces the ability to learn and form memories. In response to this early research, further studies have summarized a critical process related to learning and memory known as long term potentiation. This process relies on the stimulation of glutamate pathways in the brain (Malenka and Nicoll, 1999). Additionally, human conditions related to major disruption of learning and memory have consistently tended to be related to significant absences of glutamate neurotransmitters and receptors. Squire (1986) found reduced numbers of glutamate receptors in the hippocampus of amnesic patients, and Hyman and colleagues (1987) documented that extreme reductions in glutaminergic neurons in the entorhinal cortex and hippocampus represent a distinct feature of Alzheimer’s disease.
GABA (γ-Aminobutyric Acid)
Until the discovery of benzodiazepines, GABA had been relatively ignored in terms of its affects on learning and memory processes. Benzodiazepines were eventually found to drive activity of GABA at one of its various types of receptors (GABAA), as well as produce dramatic learning impairments (Lister, 1985). McGaugh (1989) used local administration of GABA producing compounds (agonists) or inhibiting compounds (antagonists) demonstrating they could selectively produce learning and memory impairments or enhancements depending on whether they used the GABA agonist (learning and memory impairments) or GABA antagonists (learning and memory enhancements). This body of research suggests GABA’s inhibitory nature. Specifically, a reduction of GABA in the synapse or great inhibition of the release of GABA can increase rates of firing between cells leading to greater long term potentiation and thus learning and memory consolidation.
Studies using pharmachological methods to reduce the amount of acetylcholine in the synapse (by way of compounds that inhibit acetylcholine, or compounds that completely block acetylcholine receptors) within human learning tasks and animal models have found cognitive impairment related to learning and memory (Deutsch, 1983, Coyle et al., 1983). Chapoutier (1989) additionally found that memory impairment in individuals with Parkinson’s disease is correlated with acetylcholine functioning in the frontal cortex. Winson (1990) has provided evidence that acetylcholine function can modulate rhythmic electrical brain activity (specifically in the theta and gamma frequencies) that are important for producing optimal firing rates leading to long term potentiation.
Catecholamines and Serotonin
Catecholamine systems such as epinephrine, norepinephrine and dopamine have been documented to be recruited during spatial learning and memory recall, and blockage of acetylcholine release has been demonstrated to reduce catecholamine system function (Brandeis, Brandys & Yehuda, 1989). Hatfield and McGaugh (1999) also demonstrated using a water maze task depletion of noradrenaline affected consolidation processes making the memory trace less stable (worse later recall) and more susceptible to interference. Other chemical compounds that act as neurotransmitters to bind with receptor sites have been demonstrated to play a role in memory consolidation and recall (D’Hooge & De Deyn, 2001) suggesting many different systems work together and in opposition to modulate our ability to encode and consolidate long term memories.
EMOTIONS AND FALSE MEMORIES
A flashbulb memory is a highly detailed, exceptionally vivid episodic memory of the circumstances surrounding a piece of surprising, consequential, or emotionally arousing news was heard. However, even flashbulb memories can have decreased accuracy with the passage of time, even with very important events. For example, on at least three occasions, when asked how he heard about the terrorist attacks of 9/11, President George W. Bush responded inaccurately. In January 2002, less than 4 months after the attacks, the then sitting President Bush was asked how he heard about the attacks. He responded:
I was sitting there, and my Chief of Staff—well, first of all, when we walked into the classroom, I had seen this plane fly into the first building. There was a TV set on. And you know, I thought it was pilot error and I was amazed that anybody could make such a terrible mistake. (Greenberg, 2004, p. 2)
Contrary to what President Bush recalled, no one saw the first plane hit, except people on the ground near the twin towers. The first plane was not videotaped because it was a normal Tuesday morning in New York City, until the first plane hit.
Some people attributed Bush’s wrong recall of the event to conspiracy theories. However, there is a much more benign explanation: human memory, even flashbulb memories, can be frail. In fact, memory can be so frail that we can convince a person an event happened to them, even when it did not. In a study, participants were given a list of 15 sleep-related words, but the word “sleep” was not on the list. Participants recalled hearing the word “sleep” even though they did not actually hear it (Roediger & McDermott, 2000). The researchers who discovered this named the theory after themselves and a fellow researcher, calling it the Deese-Roediger-McDermott paradigm.
Beginning with Karl Lashley, researchers and psychologists have been searching for the engram, which is the physical trace of memory. Lashley did not find the engram, but he did suggest that memories are distributed throughout the entire brain rather than stored in one specific area. Now we know that three brain areas do play significant roles in the processing and storage of different types of memories: cerebellum, hippocampus, and amygdala. The cerebellum’s job is to process procedural memories; the hippocampus is where new memories are encoded; the amygdala helps determine what memories to store, and it plays a part in determining where the memories are stored based on whether we have a strong or weak emotional response to the event. Strong emotional experiences can trigger the release of neurotransmitters, as well as hormones, which strengthen memory, so that memory for an emotional event is usually stronger than memory for a non-emotional event. This is shown by what is known as the flashbulb memory phenomenon: our ability to remember significant life events. However, our memory for life events (autobiographical memory) is not always accurate.
Openstax Psychology text by Kathryn Dumper, William Jenkins, Arlene Lacombe, Marilyn Lovett and Marion Perlmutter licensed under CC BY v4.0. https://openstax.org/details/books/psychology
1. ________ is another name for short-term memory.
a. sensory memory
b. episodic memory
c. working memory
d. implicit memory
2. The storage capacity of long-term memory is ________.
a. one or two bits of information
b. seven bits, plus or minus two
d. essentially limitless
3. The three functions of memory are ________.
a. automatic processing, effortful processing, and storage
b. encoding, processing, and storage
c. automatic processing, effortful processing, and retrieval
d. encoding, storage, and retrieval
4. This physical trace of memory is known as the ________.
b. Lashley effect
c. Deese-Roediger-McDermott Paradigm
d. flashbulb memory effect
5. An exceptionally clear recollection of an important event is a (an) ________.
b. arousal theory
c. flashbulb memory
d. equipotentiality hypothesis
Critical Thinking Questions:
1. What might happen to your memory system if you sustained damage to your hippocampus?
Personal Application Questions:
1. Describe a flashbulb memory of a significant event in your life.
Answers to Exercises
Critical Thinking Questions:
1. Because your hippocampus seems to be more of a processing area for your explicit memories, injury to this area could leave you unable to process new declarative (explicit) memories; however, even with this loss, you would be able to create implicit memories (procedural memory, motor learning and classical conditioning).
arousal theory: strong emotions trigger the formation of strong memories and weaker emotional experiences form weaker memories
engram: physical trace of memory
equipotentiality hypothesis: some parts of the brain can take over for damaged parts in forming and storing memories
flashbulb memory: exceptionally clear recollection of an important event