Item-location binding in working memory: Is it hippocampus-dependent?

A general consensus is emerging that the hippocampus has an important and active role in the creation of new long-term memory representations of associations or bindings between elements. However, it is less clear whether this contribution can be extended to the creation of temporary bound representations in working memory, involving the retention of small numbers of items over short delays. We examined this by administering a series of recognition and recall tests of working memory for color-location binding and object-location binding to a patient with highly selective hippocampal damage (Jon), and groups of control participants. Jon achieved high levels of accuracy in all working memory tests of recognition and recall binding across retention intervals of up to 10 seconds. In contrast, Jon performed at chance on an unexpected delayed test of the same object-location binding information. These findings indicate a clear dissociation between working memory and long-term memory, with no evidence for a critical hippocampal contribution to item-location binding in working memory

The neurochemistry of learning and memory.

The neurochemical basis of memory has been approached experimentally in four different ways: the bioassay; the interventive approach; the interventive-correlative approach; and the correlative approach. These approaches are fundamentally similar to those used for the study of the chemistry of any behavior. Each of these approaches has serious limitations, and significant progress has only been made by combinations of more than one. I shall discuss each of these approaches in turn

Competitive Trace Theory: A Role for the Hippocampus in Contextual Interference during Retrieval.

Much controversy exists regarding the role of the hippocampus in retrieval. The two dominant and competing accounts have been the Standard Model of Systems Consolidation (SMSC) and Multiple Trace Theory (MTT), which specifically make opposing predictions as to the necessity of the hippocampus for retrieval of remote memories. Under SMSC, memories eventually become independent of the hippocampus as they become more reliant on cortical connectivity, and thus the hippocampus is not required for retrieval of remote memories, only recent ones. MTT on the other hand claims that the hippocampus is always required no matter the age of the memory. We argue that this dissociation may be too simplistic, and a continuum model may be better suited to address the role of the hippocampus in retrieval of remote memories. Such a model is presented here with the main function of the hippocampus during retrieval being "recontextualization," or the reconstruction of memory using overlapping traces. As memories get older, they are decontextualized due to competition among partially overlapping traces and become more semantic and reliant on neocortical storage. In this framework dubbed the Competitive Trace Theory (CTT), consolidation events that lead to the strengthening of memories enhance conceptual knowledge (semantic memory) at the expense of contextual details (episodic memory). As a result, remote memories are more likely to have a stronger semantic representation. At the same time, remote memories are also more likely to include illusory details. The CTT is a novel candidate model that may provide some resolution to the memory consolidation debate

On the role of the hippocampus in the acquisition, long-term retention and semanticisation of memory

Institute for Adaptive and Neural ComputationA consensus on how to characterise the anterograde and retrograde memory processes that are lost or spared after hippocampal damage has not been reached. In this thesis, I critically re-examine the empirical literature and the assumptions behind current theories. I formulate a coherent view of what makes a task hippocampally dependent at acquisition and how this relates to its long-term fate. Findings from a neural net simulation indicate the plausibility of my proposals. My proposals both extend and constrain current views on the role of the hippocampus in the rapid acquisition of information and in learning complex associations. In general, tasks are most likely to require the hippocampus for acquisition if they involve rapid, associative learning about unfamiliar, complex, low salience stimuli. However, none of these factors alone is sufficient to obligatorily implicate the hippocampus in acquisition. With the exception of associations with supra-modal information that are always dependent on the hippocampus, it is the combination of factors that is important. Detailed, complex information that is obligatorily hippocampally-dependent at acquisition remains so for its lifetime. However, all memories are semanticised as they age through the loss of detailed context-specific information and because generic cortically-represented information starts to dominate recall. Initially hippocampally dependent memories may appear to become independent of the hippocampus over time, but recall changes qualitatively. Multi-stage, lifelong post-acquisition memory processes produce semanticised re-representations of memories of differing specificity and complexity, that can serve different purposes. The model simulates hippocampal and cortical interactions in the acquisition and maintenance of episodic and semantic events, and behaves in accordance with my proposals. In particular, conceptualising episodic and semantic memory as representing points on a continuum of memory types appears viable. Support is also found for proposals on the relative importance of the hippocampus and cortex in the rapid acquisition of information and the acquisition of complex multi-model information; and the effect of existing knowledge on new learning. Furthermore, episodic and semantic events become differentially dependent on cortical and hippocampal components. Finally, as a memory ages, it is automatically semanticised and becomes cortically dependent

A cognitive chameleon: lessons from a novel MAPT mutation case.

We report a case of frontotemporal dementia caused by a novel MAPT mutation (Q351R) with a remarkably long amnestic presentation mimicking familial Alzheimer's disease. Longitudinal clinical, neuropsychological and imaging data provide convergent evidence for predominantly bilateral anterior medial temporal lobe involvement consistent with previously established neuroanatomical signatures of MAPT mutations. This case supports the notion that the neural network affected in MAPT mutations is determined to a large extent by the underlying molecular pathology. We discuss the diagnostic significance of anomia in the context of atypical amnesia and the impact of impaired episodic and semantic memory systems on autobiographical memory