Recent studies have demonstrated that memory performance can be enhanced by a cue which indicates the item most likely to be subsequently probed, even when that cue is delivered seconds after a stimulus array is extinguished. Although such retro-cuing has attracted considerable interest, the mechanisms underlying it remain unclear. Here, we tested the hypothesis that retro-cues might protect an item from degradation over time. We employed two techniques that previously have not been deployed in retro-cuing tasks. First, we used a sensitive, continuous scale for reporting the orientation of a memorized item, rather than binary measures (change or no change) typically used in previous studies. Second, to investigate the stability of memory across time, we also systematically varied the duration between the retro-cue and report. Although accuracy of reporting uncued objects rapidly declined over short intervals, retro-cued items were significantly more stable, showing negligible decline in accuracy across time and protection from forgetting. Retro-cuing an object’s color was just as advantageous as spatial retro-cues. These findings demonstrate that during maintenance, even when items are no longer visible, attention resources can be selectively redeployed to protect the accuracy with which a cued item can be recalled over time, but with a corresponding cost in recall for uncued items.

Some prominent studies have claimed that the medial temporal lobe is not involved in retention of information over brief intervals of just a few seconds. However, in the last decade several investigations have reported that patients with medial temporal lobe damage exhibit an abnormally large number of errors when required to remember visual information over brief intervals. But the nature of the deficit and the type of error associated with medial temporal lobe lesions remains to be fully established. Voltage-gated potassium channel complex antibody-associated limbic encephalitis has recently been recognized as a form of treatable autoimmune encephalitis, frequently associated with imaging changes in the medial temporal lobe. Here, we tested a group of these patients using two newly developed visual short-term memory tasks with a sensitive, continuous measure of report. These tests enabled us to study the nature of reporting errors, rather than only their frequency. On both paradigms, voltage-gated potassium channel complex antibody patients exhibited larger errors specifically when several items had to be remembered, but not for a single item. Crucially, their errors were strongly associated with an increased tendency to report the property of the wrong item stored in memory, rather than simple degradation of memory precision. Thus, memory for isolated aspects of items was normal, but patients were impaired at binding together the different properties belonging to an item, e.g. spatial location and object identity, or colour and orientation. This occurred regardless of whether objects were shown simultaneously or sequentially. Binding errors support the view that the medial temporal lobe is involved in linking together different types of information, potentially represented in different parts of the brain, regardless of memory duration. Our novel behavioural measures also have the potential to assist in monitoring response to treatment in patients with memory disorders, such as those with voltage-gated potassium channel complex antibody limbic encephalitis.

Long-term episodic memory deficits in Alzheimer's disease (AD) are well characterised but, until recently, short-term memory (STM) function has attracted far less attention. We employed a recently-developed, delayed reproduction task which requires participants to reproduce precisely the remembered location of items they had seen only seconds previously. This paradigm provides not only a continuous measure of localization error in memory, but also an index of relational binding by determining the frequency with which an object is misplaced to the location of one of the other items held in memory. Such binding errors in STM have previously been found on this task to be sensitive to medial temporal lobe (MTL) damage in focal lesion cases. Twenty individuals with pathological mutations in presenilin 1 or amyloid precursor protein genes for familial Alzheimer's disease (FAD) were tested together with 62 healthy controls. Participants were assessed using the delayed reproduction memory task, a standard neuropsychological battery and structural MRI.Overall, FAD mutation carriers were worse than controls for object identity as well as in gross localization memory performance. Moreover, they showed greater misbinding of object identity and location than healthy controls. Thus they would often mislocalize a correctly-identified item to the location of one of the other items held in memory. Significantly, asymptomatic gene carriers – who performed similarly to healthy controls on standard neuropsychological tests – had a specific impairment in object-location binding, despite intact memory for object identity and location. Consistent with the hypothesis that the hippocampus is critically involved in relational binding regardless of memory duration, decreased hippocampal volume across FAD participants was significantly associated with deficits in object-location binding but not with recall precision for object identity or localization. Object-location binding may therefore provide a sensitive cognitive biomarker for MTL dysfunction in a range of diseases including AD.

Although we frequently take advantage of memory for objects locations in everyday life, understanding how an object’s identity is bound correctly to its location remains unclear. Here we examine how information about object identity, location and crucially object-location associations are differentially susceptible to forgetting, over variable retention intervals and memory load. In our task, participants relocated objects to their remembered locations using a touchscreen. When participants mislocalized objects, their reports were clustered around the locations of other objects in the array, rather than occurring randomly. These ‘swap’ errors could not be attributed to simple failure to remember either the identity or location of the objects, but rather appeared to arise from failure to bind object identity and location in memory. Moreover, such binding failures significantly contributed to decline in localization performance over retention time. We conclude that when objects are forgotten they do not disappear completely from memory, but rather it is the links between identity and location that are prone to be broken over time.

Reports have conflicted about the possible special role of location in visual working memory (WM). One important question is: Do we maintain the locations of objects in WM even when they are irrelevant to the task at hand? Here we used a continuous response scale to study the types of reporting errors that participants make when objects are presented at the same or at different locations in space. When several objects successively shared the same location, participants exhibited a higher tendency to report features of the wrong object in memory; that is, they responded with features that belonged to objects retained in memory but not probed at retrieval. On the other hand, a similar effect was not observed when objects shared a nonspatial feature, such as color. Furthermore, the effect of location on reporting errors was present even when its manipulation was orthogonal to the task at hand. These findings are consistent with the view that binding together different nonspatial features of an object in memory might be mediated through an object’s location. Hence, spatial location may have a privileged role in WM. The relevance of these findings to conceptual models, as well as to neural accounts of visual WM, is discussed.Electronic supplementary materialThe online version of this article (doi:10.3758/s13414-013-0541-y) contains supplementary material, which is available to authorized users.