An associative analysis of object memory

Ward-Robinson, Jasper; Bonardi, Charlotte

doi:10.1016/j.bbr.2014.10.046

Cited by 13 publications

(16 citation statements)

References 76 publications

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“…The transgenic mice performed significantly worse than the wild types on two of the four minutes of the test, and overall -in contrast to the wild type animals -showed no significant preference for the displaced objects. In contrast, in Experiment 1 mice of the same age were not significantly impaired on a relative recency task, supposedly a measure of self-generated priming [52]. In both experiments the transgenic mice performed normally on the SOR task, mirroring previous work using animals of this age [40,42].…”

Section: Discussionsupporting

confidence: 62%

“…Although SOR performance is typically unaffected in this model at this age, it was argued that according to one specific model of recognition memory, SOP [45], performance on SOR depends on two independent cognitive mechanisms: self-generated and retrieval-generated priming [52]. Thus even if one of these mechanisms were impaired, SOR performance could appear unaffected provided the other remained intact enough to support accurate performance.…”

Section: Discussionmentioning

confidence: 99%

“…Experiment 2 employed an object-in-place (OIP) task [56], which has been argued to provide a pure measure of the retrieval-generated priming process [52]. In the sample phase four different items were presented in an array; in the subsequent test, two of the items remained in their original positions while the remaining two items exchanged locations.…”

Section: Methodsmentioning

confidence: 99%

“…This is an influential theory of associative learning [45] that has proved effective in predicting and explaining a wide variety of learning phenomena [46,47,48]. Because SOP is unique in explaining associative learning through a specific conceptualisation of memory, it has also been successfully applied to recognition memory [49,50,51,52,53]. SOP asserts that any stimulus may be regarded as a set of elements.…”

Section: Introductionmentioning

confidence: 99%

“…According to this analysis both self-and retrieval-generated priming may contribute to performance on the SOR task [52]. Initial presentation of the preexposed object will prime its elements into A1, from where they decay into A2.…”

Section: Introductionmentioning

confidence: 99%

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Deficits in object-in-place but not relative recency performance in the APPswe/PS1dE9 mouse model of Alzheimer’s disease: Implications for object recognition

Bonardi

Pardon

Armstrong

2016

Behavioural Brain Research

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Performance was examined on three variants of the spontaneous object recognition (SOR) task, in 5-month old APPswe/PS1dE9 mice and wild-type littermate controls. A deficit was observed in an object-in-place (OIP) task, in which mice are preexposed to four different objects in specific locations, and then at test two of the objects swap locations (Experiment 2). Typically more exploration is seen of the objects which have switched location, which is taken as evidence of a retrieval-generated priming mechanism. However, no significant transgenic deficit was found in a relative recency (RR) task (Experiment 1), in which mice are exposed to two different objects in two separate sample phases, and then tested with both objects. Typically more exploration of the firstpresented object is observed, which is taken as evidence of a self-generated priming mechanism. Nor was there any impairment in the simplest variant, the spontaneous object recognition (SOR) task, in which mice are preexposed to one object and then tested with the familiar and a novel object. This was true regardless of whether the sample-test interval was 5 minutes (Experiment 1) or 24 hours (Experiments 1 and 2). It is argued that SOR performance depends on retrieval-generated priming as well as self-generated priming, and our preliminary evidence suggests that the retrieval-generated priming process is especially impaired in these young transgenic animals . 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 The aim of our research has been to identify early cognitive signs of AD in one specific genetic model, the double-transgenic APPswe/PS1dE9 mouse. This may be the best-characterised transgenic model of AD to date, co-expressing the mutated Swedish APP gene and also the exon-9 deleted variant of the PS1 gene [5]. Elevated levels of oligomeric Aβ in the cortex and hippocampus have been observed at 3.5 months of age in these mice; these changes are accompanied by synaptic deficits [6,7], and are also closely associated with swollen dystrophic cholinergic neurites [8].Although the amyloid plaques characteristic of AD have been reported at 4 months of age in these mice, it is only from 6 months that they are consistently observed [9]. Aβ deposition is paralleled by progressive degeneration of monaminergic [10,11] and striatal [12] neurons, and neuroinflammatory reactions [13] which mirror human AD pathology. These animals also recapitulate the age-related cognitive decline characteristic of AD [14], which is thought to depend on these neuropathological changes.The neuropathology that develops in AD in general, and in this mouse model in particular, is well specified. But precisely which aspects of this brain pathology underlie the cognitive deficits that are such a central feature of AD is still under debate [15]. In this particular mouse line, some...

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%