Memories aren’t stored in just one part of the brain.

Different types are stored across different,

interconnected brain regions. For explicit memories – which are about events that happened to you
(episodic), as well as general facts and information (semantic) – there are three important areas of the
brain: the hippocampus, the neocortex and the amygdala. Implicit memories, such as motor memories,
rely on the basal ganglia and cerebellum. Short-term working memory relies most heavily on the
prefrontal cortex.

Explicit memory
There are three areas of the brain involved in explicit memory: the hippocampus, the neo-
cortex and the amygdala.
Hippocampus
The hippocampus, located in the brain's temporal lobe, is where episodic memories are
formed and indexed for later access. Episodic memories are autobiographical memories from
specific events in our lives, like the coffee we had with a friend last week.

Neocortex
The neocortex is the largest part of the cerebral cortex, the sheet of neural tissue that forms
the outside surface of the brain, distinctive in higher mammals for its wrinkly appearance. In
humans, the neocortex is involved in higher functions such as sensory perception, generation
of motor commands, spatial reasoning and language. Over time, information from certain
memories that are temporarily stored in the hippocampus can be transferred to the neocortex
as general knowledge – things like knowing that coffee provides a pick-me-up. Researchers
think this transfer from hippocampus to neocortex happens as we sleep.
Amygdala
The amygdala, an almond-shaped structure in the brain’s temporal lobe, attaches emotional
significance to memories. This is particularly important because strong emotional memories
(e.g. those associated with shame, joy, love or grief) are difficult to forget. The permanence
of these memories suggests that interactions between the amygdala, hippocampus and
neocortex are crucial in determining the ‘stability’ of a memory – that is, how effectively it is
retained over time.
There's an additional aspect to the amygdala’s involvement in memory. The amygdala doesn't
just modify the strength and emotional content of memories; it also plays a key role
in forming new memories specifically related to fear. Fearful memories are able to be formed
after only a few repetitions. This makes ‘fear learning’ a popular way to investigate the
mechanisms of memory formation, consolidation and recall. Understanding how the
amygdala processes fear is important because of its relevance to post-traumatic stress
disorder (PTSD), which affects many of our veterans as well as police, paramedics and others
exposed to trauma. Anxiety in learning situations is also likely to involve the amygdala, and
may lead to avoidance of particularly challenging or stressful tasks.
QBI researchers including Professor Pankaj Sah and Dr Timothy Bredy believe that
understanding how fear memories are formed in the amygdala may help in treating conditions
such as post-traumatic stress disorder.
Implicit memory
There are two areas of the brain involved in implicit memory: the basal ganglia and the
cerebellum.
Basal ganglia
The basal ganglia are structures lying deep within the brain and are involved in a wide range
of processes such as emotion, reward processing, habit formation, movement and learning.
They are particularly involved in co-ordinating sequences of motor activity, as would be
needed when playing a musical instrument, dancing or playing basketball. The basal ganglia
are the regions most affected by Parkinson’s disease. This is evident in the impaired
movements of Parkinson’s patients.
Cerebellum
The cerebellum, a separate structure located at the rear base of the brain, is most important in
fine motor control, the type that allows us to use chopsticks or press that piano key a fraction
more softly. A well-studied example of cerebellar motor learning is the vestibulo-ocular
reflex, which lets us maintain our gaze on a location as we rotate our heads.
Working memory
Prefrontal cortex
The prefrontal cortex (PFC) is the part of the neocortex that sits at the very front of the brain.
It is the most recent addition to the mammalian brain, and is involved in many complex
cognitive functions. Human neuroimaging studies using magnetic resonance imaging
(MRI) machines show that when people perform tasks requiring them to hold information in
their short-term memory, such as the location of a flash of light, the PFC becomes active.
There also seems to be a functional separation between left and right sides of the PFC: the
left is more involved in verbal working memory while the right is more active in spatial
working memory, such as remembering where the flash of light occurred.

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.
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

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.
In this TED Talk, Steve Ramirez and Xu Liu from MIT talk about using laser
beams to manipulate fear memory in rats.

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 (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.

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

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.