Online research in philosophy

Aggleton & Brown rightly point out the shortcomings of the medial temporal lobe hypothesis as an approach to anterograde amnesia. Their broader perspective is a necessary corrective, and one hopes it will be taken very seriously. Although they correctly note the dangers of conflating recognition and recall, they themselves make a similar mistake in discussing familiarity; we suggest an alternative approach. We also discuss implications of their view for an analysis of retrograde amnesia. The notion that there are two routes by which the hippocampus can reactivate neuronal ensembles in the neocortex could help us understand some currently puzzling facts about the dynamics of memory consolidation.

This commentary provides a critique of Tsuda's target article, focusing on the hippocampus and episodic long-term memory. More specifically, the relevance of Cantor coding and chaotic itinerancy for long-term memory functioning is considered, given what we know about the involvement of the hippocampus in the mediation of long-term episodic memory (based on empirical neuroimaging studies and investigations of brain-damaged amnesic patients).

My aim in this paper is to show that consciousness entails self-consciousness by focusing on the relationship between consciousness and memory. More specifically, I addreess the following questions: (1) does consciousness require episodic memory?; and (2) does episodic memory require self-consciousness? With the aid of some Kantian considerations and recent empirical data, it is argued that consciousness does require episodic memory. This is done after defining episodic memory and distinguishing it from other types of memory. An affirmative answer to (2) is also warranted especially in the light of the issues raised in answering (1). I claim that 'consciousness entails self-consciousness' is thereby shown via the route through episodic memory, i.e. via affirmative answers to (1) and (2). My aim is to revive this Kantian thesis and to bring together current psychological research on amnesia with traditional philosophical perspectives on consciousness and memory.

Three questions arising from Aggleton & Brown's target article are addressed. (1) Is there any benefit to considering the effects of partial lesions of the anterior thalamic nuclei (AT)? (2) Do the AT have a separate role in the proposed extended hippocampal system? (3) Should perirhinal cortex function be restricted to familiarity judgements?

The goal of our target article was to review a number of emerging facts about the effects of limbic damage on memory in humans and animals, and about divisions within recognition memory in humans. We then argued that this information can be synthesized to produce a new view of the substrates of episodic memory. The key pathway in this system is from the hippocampus to the anterior thalamic nuclei. There seems to be a general agreement that the importance of this pathway has previously been underestimated and that it warrants further study. At the same time, a number of key questions remain. These concern the relationship of this system to another temporal-lobe/diencephalic system that contributes to recognition, and the relationship of these systems to prefrontal cortex activity.

We applaud Aggleton & Brown's affirmation of limbic diencephalic-hippocampal interaction as a key memory substrate. However, we do not agree with a thesis of diencephalic-hippocampal strict dedication to episodic memory. Instead, this circuitry supports the production of context-specific patterns of activation that subserve retrieval for a broad class of memory phenomena, including goal-directed instrumental behavior of animals and episodic memory of humans.

Three comments are made. The proposal that recollection and familiarity-based recognition take different thalamic routes does not fit recent experimental evidence, suggesting that mediodorsal thalamus acts in an integrative role with respect to prefrontal cortex. Second, the role of frontal cortex in episodic memory has been understated. Third, the role of the hippocampal axis is likely to be the computation and storage of ideothetic information.

Aggleton & Brown have built a convincing case that hippocampus-related circuits may be involved in thalamic amnesia. It remains to be established, however, that their model represents a distinct neurological system, that the distinction between recall and familiarity captures the roles of these pathways in episodic memory, or that there are no other systems that contribute to the signs of amnesia associated with thalamic disease.

Aggleton & Brown (A&B) propose that the hippocampal-anterior thalamic and perirhinal-medial dorsal thalamic systems play independent roles in episodic memory, with the hippocampus supporting recollection-based memory and the perirhinal cortex, recognition memory. In this commentary we discuss whether there is experimental support for the A&B model from studies of long-term memory in semantic dementia.