8.2 Parts of the Brain Involved in Memory

THE AMYGDALA

   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 HIPPOCAMPUS

   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).

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 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.

Glutamate

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 (GABA_A), 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.

Acetylcholine

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