Between-systems memory interference model: Difference between revisions

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== Between-Systems Memory Interference Model ==

=== Summary ===

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=== 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 <ref name="post">{{cite book|last=Kolb|first=Bryan|title=Fundamentals of Human Neuropsychology|year=2009|publisher=Worth Publishers|___location=New York: NY|edition=6th|coauthors=Whishaw, Ian Q.}}</ref> 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 <ref>{{cite journal|last=Sparks|first=F.T.|coauthors=Lehmann, H., Sutherland, R.J.|title=Between-systems memory interference during retrieval|journal=European Journal of Neuroscience|year=2011|volume=34|page=780–786|doi=10.1111/j.1460-9568.2011.07796.x|issue=5}}</ref>

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 <ref name="test">{{cite journal|last=Lehmann|first=H|coauthors=Sparks, F.T., Spanswick, S.C., Hadikin, C., McDonald, R.J., & Sutherland, R.J.|title=Making context memories independent of the hippocampus|journal=Cold Spring Harbor Laboratory Press|year=2009|volume=16|page=417–420}}</ref>. 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 <ref name="best">{{cite journal|last=Sutherland|first=R.J.|coauthors=Lehmann, H., Spanswick, S.C., Sparks, F.T., & Melvin, N.R.|title=Growth points in research on memory and hippocampus|journal=Canadian Journal of Experimental Psychology|year=2006|volume=60|page=166–174|doi=10.1037/cjep20060016|issue=2}}</ref>. The mechanism of this [[interference theory|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<ref>{{cite journal|last=Biedenkapp|first=J.C.|coauthors=Rudy, J.W.|title=Hippocampal and extra-hippocampal systems compete for control of contextual fear: Role of ventral subiculum and amygdala|journal=Learning & Memory|year=2009|volume=16|page=38–45|doi=10.1101/lm.1099109}}</ref>. 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 .<ref name="test" /> <ref name="best" />. 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 <ref name="test" />.

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)<ref name="test" /> 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 <ref name="best" />. Conversely another view is that memories become independent of the HPC over time due to a reorganization of stored memories <ref name="test" /> <ref>{{cite journal|last=Squires|first=L.R.|coauthors=Bayley, P.J.|title=The neuroscience of remote memory|journal=Current Opinion in Neurobiology|year=2007|volume=17|page=185–196|doi=10.1016/j.conb.2007.02.006|issue=2}}</ref>. 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 .<ref>{{cite journal|last=Moscovitch|first=M|coauthors=Nadel, I., Winocur, G., Gilboa, A., & Rosenbaum, R.S|title=The cognitive neuroscience of remote episodic, semantic and spatial memory|journal=Current Opinion in Neurobiology|year=2006|volume=5|page=179–190|doi=10.1016/j.conb.2006.03.013|issue=2}}</ref>.

=== Procedure ===

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Using this paradigm, the rats were [[Bilateral symmetry|bilaterally]] injected with either [[muscimol]] or [[Physiological saline|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|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 [[Lesion|lesionedlesion]]ed before the [[fear conditioning]] trial. They found that rats receiving damage after conditioning demonstrated less [[Freezing behavior|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 amnesia|retrograde]], but not [[anterograde amnesia]].

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

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There were four total groups in this paradigm. First, the control group (Saline-Saline) were administered with saline right before the [[Learning|acquisition]] of the memory and again before the [[Memory retention|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 (Mucsimol-Saline) was the most crucial to this study, as results demonstrated that mucsimol 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-mucsimol) allowed the researchers to mimic the effects of post-training hippocampal lesions, where rats were administered with saline prior to acquisition and mucsimol 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 past memories, may be seen as the hippocampus interfering with the retrieval of memories from the non-hippocampal systems <ref name="post" /> <ref name="best" />. 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.

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{{reflist}}

==References==

== References ==

* Sparks, Fraser; Lehmann H., Sutherland R.J. (2011). "Between-systems memory interference during retrieval". European Journal of Neuroscience 34 (34): 780–786. doi:10.1111/j.1460-9568.2011.07796.x.

* Kolb, Bryan; Whishaw, Ian Q. (2009). Fundamentals of Human Neuropsychology (6th ed.). New York: NY: Worth Publishers.

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[[Cateogory:Interference Theory]

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