Stimulus context and satiation.

Kivy, Peter; Earl, Robert W.; Walker, Edward T.

doi:10.1037/h0040984

Cited by 62 publications

(46 citation statements)

References 2 publications

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“…On the basis of previous response to change studies (e.,;., Kivy, Earl & Walker, 1956;Dember, 1956) it was expected that more Ss would enter the changed arm on trial one then would enter the unchanged arm. On the first test trial, 13 out of .15 entered the changed arm in Experiment I, 12 out of 16 in Experiment II, and 10 out of 11 in Experiment III.…”

Section: Results and Dlseusslonmentioning

confidence: 99%

Visual stimulus complexity and food vs. food alone as rewards for rats

1965

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Section: Results and Dlseusslonmentioning

confidence: 99%

Visual stimulus complexity and food vs. food alone as rewards for rats

1965

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“…Thus it has been suggested that visual recognition deficits might be a diagnostic marker of the early stages of AD [28,29]. In non-human animals this type of memory is assessed in the spontaneous object recognition task (SOR), which exploits the observation that rodents will preferentially explore a novel object in preference to one that is familiar [30,31]. Animals are exposed to a pair of identical, junk objects, and then after a retention interval returned to the apparatus, where one of the preexposed objects has been replaced with a novel item.…”

Section: Introductionmentioning

confidence: 99%

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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“…While several investigators, including Glanzer (1953), Walker, Dember, Earl, &Karoly (1955), andO'Connell (1964), cIaimed to have found alternation ofvisual stimuli, Douglas (1966)has concluded that only odor trail and spatial direction are effective as cues for alternation. This assertion seems doubtful in view of the fact that brightness has been shown to be a critica1 factor in experiments involving stimulus change (Dember, 1956;Dember & Millbrook, 1956;Kivy, Earl, & Walker, 1956;O'Connell, 1964) and exploration (Montgomery, 1953), two phenomena that are c10sely related to spontaneous alternation behavior. Accordingly, the present experiment attempted to assess the relative contribution of visual and spatial-direction cues for alternation with odor-trail cues eliminated.…”

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confidence: 76%