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#REDIRECT [[Hippocampus#Between-systems memory interference model]]
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== Between-Systems Memory Interference Model ==
=== Summary ===
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 <ref>{{cite journal|last=Sparks|first=Fraser|coauthors=Lehmann H., Sutherland R.J.|title=Between-systems memory interference during retrieval|journal=European Journal of Neuroscience|year=2011|issue=34|pages=780–786|doi=10.1111/j.1460-9568.2011.07796.x|volume=34}}</ref> 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, [[Engram (neuropsychology)|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.
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=== Procedure ===
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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 [[Fear conditioning|contextual fear conditioning]] paradigm allowed Fraser Sparks, Hugo Lehmann, and Robert Sutherland <ref>{{cite journal|last=Sparks|first=Fraser|coauthors=Lehmann H., Sutherland R.J.|title=Between-systems memory interference during retrieval|journal=European Journal of Neuroscience|year=2011|issue=36|pages=780–786}}</ref> to further investigate their model. They began by allowing their rat subjects to freely explore the [[Operant conditioning chamber|conditioning chamber]] for three minutes, enabling them to become [[Habituation|habituated]]. Afterwards, five 1 miliAmp 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 behavior|freezing behaviour]] was measured using [http://www.coulbourn.com/SearchResults.asp?searching=Y&sort=7&search=freezeframe&show=50&page=1 FreezeFrame Video-Based Conditioned Fear System].
[[Category:Memory]]
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|lesioned]] 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.
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===
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 [[Systems neuroscience|multiple-systems model]], suggesting that some effects may not be simply mediated by one portion of the brain.
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==References==
* Sparks F.T., Lehmann H., Sutherland R.J. (2011) Between-systems memory interference during retrieval. European Journal of Neuroscience 34, 780–786.
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