Hippocampal memory encoding and retrieval

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The hippocampus participates in the encoding, consolidation, and retrieval of memories. [1] The hippocampus is located in the medial temporal lobe (subcortical), and is an infolding of the medial temporal cortex. [1] The hippocampus plays an important role in the transfer of information from short-term memory to long-term memory during encoding and retrieval stages. These stages do not need to occur successively, but are, as studies seem to indicate, and they are broadly divided in the neuronal mechanisms that they require or even in the hippocampal areas that they seem to activate. According to Gazzaniga, "encoding is the processing of incoming information that creates memory traces to be stored." [1] There are two steps to the encoding process: "acquisition" and "consolidation". During the acquisition process, stimuli are committed to short term memory. [1] Then, consolidation is where the hippocampus along with other cortical structures stabilize an object within long term memory, which strengthens over time, and is a process for which a number of theories have arisen to explain the underlying mechanism. [1] After encoding, the hippocampus is capable of going through the retrieval process. The retrieval process consists of accessing stored information; this allows learned behaviors to experience conscious depiction and execution. [1] Encoding and retrieval are both affected by neurodegenerative and anxiety disorders and epilepsy.

Contents

Theories and reasoning

HIPER (hippocampal encoding/retrieval) model

Meta-positron emission tomography (PET) analysis has lent support toward a division of the hippocampus between caudal and rostral regions. [2] Scans have demonstrated a uniform variation in blood flow distribution within the hippocampus (and the medial temporal lobe broadly) during the separate processes of episodic encoding and retrieval. [2] In the hippocampal encoding/retrieval (HIPER) model, episodic encoding is found to take place within the rostral region of the hippocampus whereas retrieval takes place in the caudal region. [2] However, the divide between these regions need not be disjoint, as functional magnetic resonance imaging (fMRI) data has demonstrated encoding processes occurring within the caudal region. [2]

HIPER is a model resulting from and therefore a reflection of certain experimental phenomena, but cannot completely explain hippocampal encoding and retrieval on its own. [2] Nevertheless, the model suggests a broad division of labor in encoding and retrieval, whether they involve separate regions of the hippocampus or act simultaneously or independently within a single, more inclusive process.

Theta phase separation

In a framework first developed by Hasselmo and colleagues, theta phase separation implies that the theta rhythm of the hippocampus occurs in cycles and various phases of the rhythm entail encoding and retrieval as separate processes. [3] [4] An extra-hippocampal structure, the septum, initiates and regulates the theta rhythm and its associated memory processes. GABAergic activity within the septum inhibits certain classes of CA3 cells (a region of the hippocampus), the divide often drawn between basket cells, pyramidal cells, and interneurons, to distinguish encoding from retrieval mechanisms. The study emphasizes and models the CA3 subfield of the hippocampus as a primary inducement towards encoding and retrieval. Encoding as a procedure begins when septal GABAergic inhibition is at minimum, freeing basket cells to act within CA3, and during brief dis-inhibition periods, other cells receive input: a proximal entorhinal input toward pyramidal cells and a coincident dentate gyrus input toward interneurons. [3] [4] On the other hand, retrieval as a procedure begins when septal GABAergic inhibition is at maximum, occluding basket cell activity and enabling pyramidal cells to signal. [3] During this period, Oriens- Lacunosum Moleculare (O-LM) cells disambiguate memory for retrieval. [4]

CA3 is significant as it allows auto-associative processes through a recurrent, collateral system. [3] The theta phase separation model agrees generally with others on the significance of CA3 but is the first to attribute both the processes of encoding and retrieval to the subfield. [3] [4]

Reconsolidation hypothesis

The reconsolidation hypothesis claims that objects encoded into long term memory experience a new period of consolidation, or the time and resource expended to stabilize a memory object, upon each recollection. This is in opposition to the classical consolidation hypothesis which regards consolidation as a one-time event, following the first encoding of a memory. A memory item in this hypothesis, upon reactivation, destabilizes for a brief period and thereafter invokes the neuronal processes requisite for stabilization. [5]

The reconsolidation hypothesis has lingered since the 1960s; however, a 2000 study, entitled "Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval", examining fear conditioning in rats, has provided evidence in its favor. [6] After receiving post-retrieval an intra-amygdalar infusion of a known amnesic agent, anisomycin, rats failed to recall a rapidly learned fear memory. [6] Hippocampal lesions formed post-retrieval affected the rats' fear conditioning in a similar manner. [6]

The reconsolidation hypothesis does not suppose that subsequent and precedent consolidation phases are necessarily identical in duration or in the neural mechanisms involved. Nevertheless, the commonality that exists in every consolidation phase is a short-lived destabilization of a memory object and a susceptibility for said object to react to amnesic agents—principally protein synthesis inhibitors. [5] Morris and colleagues' experiment indicates that the reconsolidation hypothesis could apply to particular memory types such as allocentric spatial memory, which is either acquired slowly or rapidly. As implied by the authors, however, such an application is feasible only in the case of rapidly acquired spatial memory, the degree to which is influenced by how thoroughly a spatial object is trained. [5]

Hippocampal disorders that affect encoding and retrieval

Psychiatric disorders

Individuals who develop hippocampal lesions often fare poorly on measures of verbal declarative memory. Tests involving the recall of paragraphs or strings of words, as cited by Bremner and colleagues, illustrate a degree of dysfunction among lesion patients proportionate to the percentage of hippocampal volume and the amount of cells lost. [7]

As precursors toward later studies that would showcase the effect of post-traumatic stress disorder (PTSD) on the human hippocampus, animal studies have broadly demonstrated a susceptibility of the mammalian hippocampus to stressors. In particular, stressed animals develop functional deficits in memory, changes in hippocampal form, and an impairment in neurogenesis, or the ability to produce new neurons. [7]

Bremner and colleagues implemented MRI and PET neuroimaging to measure structure and function respectively and demonstrated a lower average hippocampal volume and activation among women with PTSD. The participants of the study included a population of women who had or had not experienced childhood sexual abuse, a certain subset among which developed PTSD. PET and MRI analysis indicated a 16% lower mean hippocampal volume among abused women who developed PTSD and a 19% lower mean hippocampal volume than all other populations in the experiment. [7]

Epilepsy

The effect of seizures on memory are often categorized with respect to their intensity and the cortical areas they affect. Epileptic patients, especially those who suffer from temporal lobe epilepsy, often experience deficits in memory encoding and retrieval, developing anterograde and retrograde amnesia. [8] At times, if a seizure specifically affects the hippocampus, the individual afflicted can encode memory; however, that memory rapidly extinguishes. [8]

Accompanying the onset of epilepsies is hippocampal sclerosis, also known as Ammon's horn sclerosis. Individuals afflicted suffer unilateral volume loss, as evidenced by MRI scans. [9] Hippocampal sclerosis involves neural loss and a selective mesial temporal sclerosis (MTS) danger and is likely caused by an overactivation of N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors by the surplus signaling of excitatory neurotransmitters. [9] The depolarization and calcium overload experienced by overactive receptors signal the expression of cell death pathways. [9]

Disease

According to the Journal of Neurology, Neurosurgery, and Psychiatry, Alzheimer's generally causes a reduction in tissue as well as neurodegeneration throughout the brain. Out of all areas in the brain, the hippocampus is among the first to be damaged by Alzheimer's. One study located in the Journal of Neurology, Neurosurgery, and Psychiatry tested to see the volume changes of the hippocampus in Alzheimer's disease patients. Results showed that there was 27% less volume in the hippocampus compared with the hippocampus found in normal cognition. Lastly, the difference between the hippocampus of an Alzheimer's patient and that of a normal patient was shown through the notable loss seen in cortical grey matter in Alzheimer's. [10]

Experiment

Methods

In an experiment performed by Zeineh and colleagues, ten subjects were scanned by fMRI while engaged in a face-name associative task that linked a sequence of faces unknown to the participants with the names of the individuals to whom they belonged. [11] The hippocampus is known to play a role in the encoding of memory that associates between a face and a name. The experiment began by dividing encoding blocks, in which the participants viewed and attempted to memorize the faces paired with the names, from retrieval blocks, in which the participants were shown only the faces and asked to match them with their names. This process was completed four times. [11] Rote rehearsal was discouraged by a distractive task administered between encoding and recall blocks. [11]

Results

The results of Zeineh and colleagues' experiment suggest that encoding and retrieval activate different regions of the hippocampus. As indicated by the authors, a study of hippocampal activity as it pertains to learning and practice has unveiled some of the cortical processes of information acquisition. [11]

Related Research Articles

<span class="mw-page-title-main">Entorhinal cortex</span> Area of the temporal lobe of the brain

The entorhinal cortex (EC) is an area of the brain's allocortex, located in the medial temporal lobe, whose functions include being a widespread network hub for memory, navigation, and the perception of time. The EC is the main interface between the hippocampus and neocortex. The EC-hippocampus system plays an important role in declarative (autobiographical/episodic/semantic) memories and in particular spatial memories including memory formation, memory consolidation, and memory optimization in sleep. The EC is also responsible for the pre-processing (familiarity) of the input signals in the reflex nictitating membrane response of classical trace conditioning; the association of impulses from the eye and the ear occurs in the entorhinal cortex.

<span class="mw-page-title-main">Hippocampus</span> Vertebrate brain region involved in memory consolidation

The hippocampus is a major component of the brain of humans and other vertebrates. Humans and other mammals have two hippocampi, one in each side of the brain. The hippocampus is part of the limbic system, and plays important roles in the consolidation of information from short-term memory to long-term memory, and in spatial memory that enables navigation. The hippocampus is located in the allocortex, with neural projections into the neocortex, in humans as well as other primates. The hippocampus, as the medial pallium, is a structure found in all vertebrates. In humans, it contains two main interlocking parts: the hippocampus proper, and the dentate gyrus.

<span class="mw-page-title-main">Place cell</span> Place-activated hippocampus cells found in some mammals

A place cell is a kind of pyramidal neuron in the hippocampus that becomes active when an animal enters a particular place in its environment, which is known as the place field. Place cells are thought to act collectively as a cognitive representation of a specific location in space, known as a cognitive map. Place cells work with other types of neurons in the hippocampus and surrounding regions to perform this kind of spatial processing. They have been found in a variety of animals, including rodents, bats, monkeys and humans.

Explicit memory is one of the two main types of long-term human memory, the other of which is implicit memory. Explicit memory is the conscious, intentional recollection of factual information, previous experiences, and concepts. This type of memory is dependent upon three processes: acquisition, consolidation, and retrieval.

Schaffer collaterals are axon collaterals given off by CA3 pyramidal cells in the hippocampus. These collaterals project to area CA1 of the hippocampus and are an integral part of memory formation and the emotional network of the Papez circuit, and of the hippocampal trisynaptic loop. It is one of the most studied synapses in the world and named after the Hungarian anatomist-neurologist Károly Schaffer.

An apical dendrite is a dendrite that emerges from the apex of a pyramidal cell. Apical dendrites are one of two primary categories of dendrites, and they distinguish the pyramidal cells from spiny stellate cells in the cortices. Pyramidal cells are found in the prefrontal cortex, the hippocampus, the entorhinal cortex, the olfactory cortex, and other areas. Dendrite arbors formed by apical dendrites are the means by which synaptic inputs into a cell are integrated. The apical dendrites in these regions contribute significantly to memory, learning, and sensory associations by modulating the excitatory and inhibitory signals received by the pyramidal cells.

<span class="mw-page-title-main">Subiculum</span> Most inferior part of the hippocampal formation

The subiculum is the most inferior component of the hippocampal formation. It lies between the entorhinal cortex and the CA1 subfield of the hippocampus proper.

<span class="mw-page-title-main">Hippocampal sclerosis</span> Medical condition

Hippocampal sclerosis (HS) or mesial temporal sclerosis (MTS) is a neuropathological condition with severe neuronal cell loss and gliosis in the hippocampus. Neuroimaging tests such as magnetic resonance imaging (MRI) and positron emission tomography (PET) may identify individuals with hippocampal sclerosis. Hippocampal sclerosis occurs in 3 distinct settings: mesial temporal lobe epilepsy, adult neurodegenerative disease and acute brain injury.

Theta waves generate the theta rhythm, a neural oscillation in the brain that underlies various aspects of cognition and behavior, including learning, memory, and spatial navigation in many animals. It can be recorded using various electrophysiological methods, such as electroencephalogram (EEG), recorded either from inside the brain or from electrodes attached to the scalp.

<span class="mw-page-title-main">Temporal lobe epilepsy</span> Chronic focal seizure disorder

In the field of neurology, temporal lobe epilepsy is an enduring brain disorder that causes unprovoked seizures from the temporal lobe. Temporal lobe epilepsy is the most common type of focal onset epilepsy among adults. Seizure symptoms and behavior distinguish seizures arising from the medial temporal lobe from seizures arising from the lateral (neocortical) temporal lobe. Memory and psychiatric comorbidities may occur. Diagnosis relies on electroencephalographic (EEG) and neuroimaging studies. Anticonvulsant medications, epilepsy surgery and dietary treatments may improve seizure control.

<span class="mw-page-title-main">Perforant path</span>

In the brain, the perforant path or perforant pathway provides a connectional route from the entorhinal cortex to all fields of the hippocampal formation, including the dentate gyrus, all CA fields, and the subiculum.

<span class="mw-page-title-main">Michael Hasselmo</span> American neuroscientist

Michael Hasselmo is an American neuroscientist and professor in the Department of Psychological and Brain Sciences at Boston University. He is the director of the Center for Systems Neuroscience and is editor-in-chief of Hippocampus (journal). Hasselmo studies oscillatory dynamics and neuromodulatory regulation in cortical mechanisms for memory guided behavior and spatial navigation using a combination of neurophysiological and behavioral experiments in conjunction with computational modeling. In addition to his peer-reviewed publications, Hasselmo wrote the book How We Remember: Brain Mechanisms of Episodic Memory.

The trisynaptic circuit or trisynaptic loop is a relay of synaptic transmission in the hippocampus. The circuit was initially described by the neuroanatomist Santiago Ramon y Cajal, in the early twentieth century, using the Golgi staining method. After the discovery of the trisynaptic circuit, a series of research has been conducted to determine the mechanisms driving this circuit. Today, research is focused on how this loop interacts with other parts of the brain, and how it influences human physiology and behaviour. For example, it has been shown that disruptions within the trisynaptic circuit lead to behavioural changes in rodent and feline models.

<span class="mw-page-title-main">Hippocampus anatomy</span>

Hippocampus anatomy describes the physical aspects and properties of the hippocampus, a neural structure in the medial temporal lobe of the brain. It has a distinctive, curved shape that has been likened to the sea-horse monster of Greek mythology and the ram's horns of Amun in Egyptian mythology. This general layout holds across the full range of mammalian species, from hedgehog to human, although the details vary. For example, in the rat, the two hippocampi look similar to a pair of bananas, joined at the stems. In primate brains, including humans, the portion of the hippocampus near the base of the temporal lobe is much broader than the part at the top. Due to the three-dimensional curvature of this structure, two-dimensional sections such as shown are commonly seen. Neuroimaging pictures can show a number of different shapes, depending on the angle and location of the cut.

Memory consolidation is a category of processes that stabilize a memory trace after its initial acquisition. A memory trace is a change in the nervous system caused by memorizing something. Consolidation is distinguished into two specific processes. The first, synaptic consolidation, which is thought to correspond to late-phase long-term potentiation, occurs on a small scale in the synaptic connections and neural circuits within the first few hours after learning. The second process is systems consolidation, occurring on a much larger scale in the brain, rendering hippocampus-dependent memories independent of the hippocampus over a period of weeks to years. Recently, a third process has become the focus of research, reconsolidation, in which previously consolidated memories can be made labile again through reactivation of the memory trace.

<span class="mw-page-title-main">Sleep and memory</span> Relationship between sleep and memory

The relationship between sleep and memory has been studied since at least the early 19th century. Memory, the cognitive process of storing and retrieving past experiences, learning and recognition, is a product of brain plasticity, the structural changes within synapses that create associations between stimuli. Stimuli are encoded within milliseconds; however, the long-term maintenance of memories can take additional minutes, days, or even years to fully consolidate and become a stable memory that is accessible. Therefore, the formation of a specific memory occurs rapidly, but the evolution of a memory is often an ongoing process.

Sharp waves and ripples (SWRs) are oscillatory patterns produced by extremely synchronised activity of neurons in the mammalian hippocampus and neighbouring regions which occur spontaneously in idle waking states or during NREM sleep. They can be observed with a variety of imaging methods, such as EEG. They are composed of large amplitude sharp waves in local field potential and produced by tens of thousands of neurons firing together within 30–100 ms window. They are some of the most synchronous oscillations patterns in the brain, making them susceptible to pathological patterns such as epilepsy.They have been extensively characterised and described by György Buzsáki and have been shown to be involved in memory consolidation in NREM sleep and the replay of memories acquired during wakefulness.

Chantal Stern is a neuroscientist who uses techniques including functional magnetic resonance imaging (fMRI) to study the brain mechanisms of memory function. She is the Director of the Brain, Behavior and Cognition program and a professor of Psychological and Brain Sciences at Boston University.After completing a degree at McGill University, she performed her doctoral research at Oxford University with Richard Passingham.

<span class="mw-page-title-main">Hippocampus proper</span> Part of the brain of mammals

The hippocampus proper refers to the actual structure of the hippocampus which is made up of three regions or subfields. The subfields CA1, CA2, and CA3 use the initials of cornu Ammonis, an earlier name of the hippocampus.

Early long-term potentiation (E-LTP) is the first phase of long-term potentiation (LTP), a well-studied form of synaptic plasticity, and consists of an increase in synaptic strength. LTP could be produced by repetitive stimulation of the presynaptic terminals, and it is believed to play a role in memory function in the hippocampus, amygdala and other cortical brain structures in mammals.

References

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  10. ↑ Du, A.; Schuff, N.; Amend, D.; Laakso, M.; Hsu, Y.; Jagust, W.; Yaffe, K.; Kramer, J.; Reed, B.; Norman, D.; Chui, H.; Weiner, M. (2001). "Magnetic resonance imaging of the entorhinal cortex and hippocampus in mild cognitive impairment and alzheimer's disease". Journal of Neurology, Neurosurgery, and Psychiatry. 71 (4): 441–447. doi:10.1136/jnnp.71.4.441. PMC   1763497 . PMID   11561025.
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