Between-systems memory interference model

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The between-systems memory interference model describes the inhibition of non-hippocampal systems of memory during concurrent hippocampal activity. Specifically, Fraser Sparks, Hugo Lehmann, and Robert Sutherland [1] found that when the hippocampus was inactive, non-hippocampal systems located elsewhere in the brain were found to consolidate memory in its place. However, when the hippocampus was reactivated, memory traces consolidated by non-hippocampal systems were not recalled, suggesting that the hippocampus interferes with long-term memory consolidation in other memory-related systems.

Contents

History

The hippocampus (HPC) plays an important role in memory processes/functioning. It is a cortical structure in the anterior medial temporal lobe which is involved in the consolidation of short-term and long-term memories, specifically for memories of spatial navigation [2] However, there are other cortical structures involved in memories which are referred to as non-HPC memory systems. The relationship between the HPC and non-HPC systems is often studied using fear conditioning, which is a form of learning where a noxious stimulus, such as an odour or shock, creates an emotional response of fear. The amygdala is often associated with these responses in fear conditioning in which conditioned stimuli can evoke emotional memories. Indirect measures of fear conditioning, such as freezing time, have been used to infer the functional levels of spatial and learning memory [3] Researchers began believing other cortical structures, aside from the HPC, were involved in memory of contextual fear conditioning, because when the HPC was extensively damaged before fear conditioning, there was only a small effect on levels of behavioural memory assessments. [4] It was deduced that other non-HPC memory systems must be involved in encoding, storing and retrieving memories during contextual fear conditioning, and that normally the HPC interferes with these processes. [5] The mechanism of this interference is not entirely known, however studies have alluded to the location of this interference. Researchers have found that during fear conditioning the HPC competes with the non-HPC memory systems in the basolateral region of the amygdala. [6] Injections of a dopamine D1 agonist SKF82958 into this area of the amygdala before a conditioning session were correlated with a decrease in the interference by the HPC, allowing non-HPC systems to form memories of the fear conditioning. Therefore, the increased dopamine to this area, inhibits amygdala functioning which includes the HPC interfering with memory encoding in non-HPC systems.

In studies of contextual fear conditioning, there are many views describing the interaction between HPC and non-HPC systems, or the transition of memories from being hippocampus dependent to independent. The HPC and non-HPC systems may acquire the same memories but if the HPC is intact, the non-HPC systems cannot independently form or retrieve these context memories. [4] [5] Therefore, the non-HPC systems appear to act like a back-up system for memories, that are only used when the main system, the HPC, is dysfunctional or absent. On the other hand, the HPC and non-HPC systems also have different functions. For example, the hippocampus is known to be important for context discrimination, while non-hippocampal systems have not shown evidence for this specific function [4]

One view for the transfer of memories from HPC-dependent to independent is that the strength of memories changes across the HPC and non-HPC systems, with damage to the HPC. In a study by Lehmann and colleagues (2009) [4] adult male rats were put through contextual fear conditioning using feet shocks. If there was HPC damage and the rats experienced 11 sessions worth of shocks in one session, retrograde amnesia resulted. However, if there was damage in the HPC and shocks were applied over many conditioning sessions, then the memory for the contextual fear conditioning was not affected. So within the numerous conditioning sessions, the memory for contextual fear conditioning may have been formed by the non-HPC memory systems. Specifically memory representations in the non-HPC systems may be strengthened and eventually become independent of the HPC, which normally overshadows/interferes with the non-HPC systems in forming representations of memories in contextual fear conditioning. [5] Conversely another view is that memories become independent of the HPC over time due to a reorganization of stored memories. [4] [7] Alternatively others believe memories change characteristics to become independent of the HPC, specifically in becoming less precise, more general and context free memories in non-HPC systems, assuming that the HPC is required for precise, detailed, contextual memories. [8]

Procedure

The procedure utilised in supporting the between-systems memory interference model was published under the title Between-systems memory interference during retrieval. Their paper explains how using the age-tested contextual fear conditioning paradigm allowed Fraser Sparks, Hugo Lehmann, and Robert Sutherland [9] to further investigate their model. They began by allowing their rat subjects to freely explore the conditioning chamber for three minutes, enabling them to become habituated. Afterwards, five 1 milliamp foot shocks lasting 2 seconds were administered with 60 seconds in between each shock. Retention of this memory was tested 11 days after the learning trials, where freezing behaviour was measured using FreezeFrame Video-Based Conditioned Fear System.

Using this paradigm, the rats were bilaterally injected with either muscimol or sterile physiological saline depending on if they were in the experimental or control condition respectively. These total hemispheric infusions were administered one hour before the conditioning trials, additionally immediately before the testing trials, allowing 30 minutes total between the end of infusion and behavioural conditioning or testing.

With this, the researchers were left with multiple experiments. In experiment 1A, the hippocampus of the rats were permanently damaged after the fear conditioning trial, while in experiment 1B, the hippocampus of the rats were lesioned before the fear conditioning trial. They found that rats receiving damage after conditioning demonstrated less freezing than control rats, whereas rats who received damaged before the conditioning trial did not differ in their freezing habits than the control rats. These results suggest that damage to the hippocampus causes retrograde, but not anterograde amnesia.

In this study specifically, they wanted to see if the hippocampus interfered with the retrieval of memory from non-hippocampal systems. Figure 1 outlines the procedures.

There were four total groups in this paradigm. First, the control group (Saline-Saline) were administered with saline right before the acquisition of the memory and again before the retention test. The second group (Muscimol-Muscimol) had muscimol administrations again just before acquisition and retention. Because muscimol treatments would cause inactivation both before the learning trial and at the time of testing, results showed that the freezing behaviours did not greatly differ from the control group. These observations allowed the researchers to infer that there is indeed a non-hippocampal system of memory at work when the hippocampus is inactivated. The third group (muscimol-Saline) was the most crucial to this study, as results demonstrated that muscimol injections immediately before acquisition and saline injections immediately before retention resulted in a significantly lower level of freezing in rats. These results would ultimately suggest that memory that was consolidated by non-hippocampal systems when the hippocampus was inactive was subsequently competing with the hippocampus once it was active again. Lastly, the fourth group (saline-muscimol) allowed the researchers to mimic the effects of post-training hippocampal lesions, where rats were administered with saline prior to acquisition and muscimol prior to retention.

Impact

Studying between-systems interference could potentially provide further insight to understanding and treating amnesia. Specifically retrograde amnesia, where there is an inability to recall memories, may be seen as the hippocampus interfering with the retrieval of memories from the non-hippocampal systems. [2] [5] If damage or inactivation of the HPC was induced and if the non-HPC systems were strengthened, perhaps these memories could be retrieved and recalled. However, before reaching this stage of application, more work needs to be done to understand the complexity of the non-HPC systems. This vein of research could potentially lead to more neuropsychological assessments to evaluate their functioning, just as there are tests for HPC functioning. Additionally, if memories can become independent of the HPC, maybe this effect is a two-way transformation pathway such that memories in contextual fear conditioning can become dependent on the HPC again.

One of the major implications that this model illustrates is the dominant effects of the hippocampus on non-hippocampal networks when information is incongruent. With this information in mind, future directions could lead towards the study of these non-hippocampal memory systems through hippocampal inactivation, further expanding the labile constructs of memory. Additionally, many theories of memory are holistically based around the hippocampus. This model could add beneficial information to hippocampal research and memory theories such as the multiple trace theory. Lastly, the between-system memory interference model allows researchers to evaluate their results on a multiple-systems model, suggesting that some effects may not be simply mediated by one portion of the brain.

Related Research Articles

<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">Amygdala</span> Each of two small structures deep within the temporal lobe of complex vertebrates

The amygdala is a paired nuclear complex present in the cerebral hemispheres of vertebrates. It is considered part of the limbic system. In primates, it is located medially within the temporal lobes. It consists of many nuclei, each made up of further subnuclei. The subdivision most commonly made is into the basolateral, central, cortical, and medial nuclei together with the intercalated cell clusters. The amygdala has a primary role in the processing of memory, decision-making, and emotional responses. The amygdala was first identified and named by Karl Friedrich Burdach in 1822.

<span class="mw-page-title-main">Limbic system</span> Set of brain structures involved in emotion and motivation

The limbic system, also known as the paleomammalian cortex, is a set of brain structures located on both sides of the thalamus, immediately beneath the medial temporal lobe of the cerebrum primarily in the forebrain.

<span class="mw-page-title-main">Fear conditioning</span> Behavioral paradigm in which organisms learn to predict aversive events

Pavlovian fear conditioning is a behavioral paradigm in which organisms learn to predict aversive events. It is a form of learning in which an aversive stimulus is associated with a particular neutral context or neutral stimulus, resulting in the expression of fear responses to the originally neutral stimulus or context. This can be done by pairing the neutral stimulus with an aversive stimulus. Eventually, the neutral stimulus alone can elicit the state of fear. In the vocabulary of classical conditioning, the neutral stimulus or context is the "conditional stimulus" (CS), the aversive stimulus is the "unconditional stimulus" (US), and the fear is the "conditional response" (CR).

<span class="mw-page-title-main">Spatial memory</span> Memory about ones environment and spatial orientation

In cognitive psychology and neuroscience, spatial memory is a form of memory responsible for the recording and recovery of information needed to plan a course to a location and to recall the location of an object or the occurrence of an event. Spatial memory is necessary for orientation in space. Spatial memory can also be divided into egocentric and allocentric spatial memory. A person's spatial memory is required to navigate around a familiar city. A rat's spatial memory is needed to learn the location of food at the end of a maze. In both humans and animals, spatial memories are summarized as a cognitive map.

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.

<span class="mw-page-title-main">Septal area</span> Area in the lower, posterior part of the medial surface of the frontal lobe

The septal area, consisting of the lateral septum and medial septum, is an area in the lower, posterior part of the medial surface of the frontal lobe, and refers to the nearby septum pellucidum.

<span class="mw-page-title-main">James McGaugh</span> American neurobiologist and author

James L. McGaugh is an American neurobiologist and author working in the field of learning and memory. He is a Distinguished Professor Emeritus in the Department of Neurobiology and Behavior at the University of California, Irvine and a fellow and founding director of the Center for the Neurobiology of Learning and Memory.

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Ribot's law of retrograde amnesia was hypothesized in 1881 by Théodule Ribot. It states that there is a time gradient in retrograde amnesia, so that recent memories are more likely to be lost than the more remote memories. Not all patients with retrograde amnesia report the symptoms of Ribot's law.

Memory and trauma is the deleterious effects that physical or psychological trauma has on memory.

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.

The neuroanatomy of memory encompasses a wide variety of anatomical structures in the brain.

The cellular transcription factor CREB helps learning and the stabilization and retrieval of fear-based, long-term memories. This is done mainly through its expression in the hippocampus and the amygdala. Studies supporting the role of CREB in cognition include those that knock out the gene, reduce its expression, or overexpress it.

<span class="mw-page-title-main">Memory</span> Faculty of mind to store and retrieve data

Memory is the faculty of the mind by which data or information is encoded, stored, and retrieved when needed. It is the retention of information over time for the purpose of influencing future action. If past events could not be remembered, it would be impossible for language, relationships, or personal identity to develop. Memory loss is usually described as forgetfulness or amnesia.

While the cellular and molecular mechanisms of learning and memory have long been a central focus of neuroscience, it is only in recent years that attention has turned to the epigenetic mechanisms behind the dynamic changes in gene transcription responsible for memory formation and maintenance. Epigenetic gene regulation often involves the physical marking of DNA or associated proteins to cause or allow long-lasting changes in gene activity. Epigenetic mechanisms such as DNA methylation and histone modifications have been shown to play an important role in learning and memory.

Many experiments have been done to find out how the brain interprets stimuli and how animals develop fear responses. The emotion, fear, has been hard-wired into almost every individual, due to its vital role in the survival of the individual. Researchers have found that fear is established unconsciously and that the amygdala is involved with fear conditioning.

Daniela Schiller is a neuroscientist who leads the Affective Neuroscience Lab at the Mount Sinai School of Medicine. She is best known for her work on memory reconsolidation, and on modification of emotional learning and memory.

The hippocampus participates in the encoding, consolidation, and retrieval of memories. The hippocampus is located in the medial temporal lobe (subcortical), and is an infolding of the medial temporal cortex. 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." There are two steps to the encoding process: "acquisition" and "consolidation". During the acquisition process, stimuli are committed to short term memory. 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. 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. Encoding and retrieval are both affected by neurodegenerative and anxiety disorders and epilepsy.

<span class="mw-page-title-main">Stephen Maren</span>

Stephen Andrew Maren is an American behavioral neuroscientist investigating the brain mechanisms of emotional memory, particularly the role context plays in the behavioral expression of fear. He has discovered brain circuits regulating context-dependent memory, including mapping functional connections between the hippocampus, prefrontal cortex, and amygdala that are involved in the expression and extinction of learned fear responses.

References

  1. ↑ Sparks, Fraser; Lehmann H.; Sutherland R.J. (2011). "Between-systems memory interference during retrieval". European Journal of Neuroscience. 34 (5): 780–786. doi:10.1111/j.1460-9568.2011.07796.x. PMID   21896061. S2CID   25745773.
  2. 1 2 Kolb, Bryan; Whishaw, Ian Q. (2009). Fundamentals of Human Neuropsychology (6th ed.). New York: NY: Worth Publishers.
  3. ↑ Sparks, F.T.; Lehmann, H.; Sutherland, R.J. (2011). "Between-systems memory interference during retrieval". European Journal of Neuroscience. 34 (5): 780–786. doi:10.1111/j.1460-9568.2011.07796.x. PMID   21896061. S2CID   25745773.
  4. 1 2 3 4 5 Lehmann, H; Sparks, F.T.; Spanswick, S.C.; Hadikin, C.; McDonald, R.J.; Sutherland, R.J. (2009). "Making context memories independent of the hippocampus". Learning & Memory. 16 (7): 417–420. doi:10.1101/lm.1385409. PMC   2704104 . PMID   19553378.
  5. 1 2 3 4 Sutherland, R.J.; Lehmann, H.; Spanswick, S.C.; Sparks, F.T.; Melvin, N.R. (2006). "Growth points in research on memory and hippocampus". Canadian Journal of Experimental Psychology. 60 (2): 166–174. doi:10.1037/cjep20060016. PMID   17133891.
  6. ↑ Biedenkapp, J.C.; Rudy, J.W. (2009). "Hippocampal and extra-hippocampal systems compete for control of contextual fear: Role of ventral subiculum and amygdala". Learning & Memory. 16 (1): 38–45. doi:10.1101/lm.1099109. PMC   2632852 . PMID   19117915.
  7. ↑ Squires, L.R.; Bayley, P.J. (2007). "The neuroscience of remote memory". Current Opinion in Neurobiology. 17 (2): 185–196. doi:10.1016/j.conb.2007.02.006. PMC   2277361 . PMID   17336513.
  8. ↑ Moscovitch, M; Nadel, I.; Winocur, G.; Gilboa, A.; Rosenbaum, R.S (2006). "The cognitive neuroscience of remote episodic, semantic and spatial memory". Current Opinion in Neurobiology. 16 (2): 179–190. doi:10.1016/j.conb.2006.03.013. PMID   16564688. S2CID   14109875.
  9. ↑ Sparks, Fraser; Lehmann H.; Sutherland R.J. (2011). "Between-systems memory interference during retrieval". European Journal of Neuroscience. 34 (36): 780–786. doi:10.1111/j.1460-9568.2011.07796.x. PMID   21896061. S2CID   25745773.
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