Abstract

ABSTRACTThe hippocampal formation and anterior thalamic nuclei form part of an interconnected network thought to support memory. A central pathway in this mnemonic network comprises the direct projections from the hippocampal formation to the anterior thalamic nuclei, projections that, in the primate brain, originate in the subicular cortices to reach the anterior thalamic nuclei by way of the fornix. In the rat brain, additional pathways involving the internal capsule have been described, linking the dorsal subiculum to the anteromedial thalamic nucleus, as well as the postsubiculum to the anterodorsal thalamic nucleus. Confirming such pathways is essential in order to appreciate how information is transferred from the hippocampal formation to the anterior thalamus and how it may be disrupted by fornix pathology. Accordingly, in the present study, pathway tracers were injected into the anterior thalamic nuclei and the dorsal subiculum of rats with fornix lesions. Contrary to previous descriptions, projections from the subiculum to the anteromedial thalamic nucleus overwhelmingly relied on the fornix. Dorsal subiculum projections to the majority of the anteroventral nucleus also predominantly relied on the fornix, although postsubicular inputs to the lateral dorsal part of the anteroventral nucleus, as well as to the anterodorsal and laterodorsal thalamic nuclei, largely involved a nonfornical pathway, via the internal capsule. © 2015 The Authors Hippocampus Published by Wiley Periodicals, Inc.

Highlights

  • Two principal brain regions implicated in anterograde amnesia, and episodic memory, are the medial temporal lobe and the medial diencephalon

  • The projections from the medial mammillary nucleus to the anterior thalamic nuclei are ipsilateral, with pars medialis providing the majority of inputs to the anteromedial thalamic nucleus, while pars lateralis largely projects to the anteroventral nucleus

  • The results include details of comparable cases that have no fornix lesions, i.e., are intact, or have significant amounts of tract sparing. These cases make it easier to appreciate any changes in labeling related to fornix damage

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Summary

Introduction

Two principal brain regions implicated in anterograde amnesia, and episodic memory, are the medial temporal lobe and the medial diencephalon. Attention has repeatedly focused on the hippocampus and the anterior thalamic nuclei, along with their reciprocal interactions (Barbizet, 1963; Delay and Brion, 1969; Parker and Gaffan, 1997; Aggleton and Brown, 1999) Both animal lesion studies and clinical data have, for example, shown how anterior thalamic damage or disconnection can mimic many of the effects of hippocampal damage, i.e., causing memory loss in humans and spatial deficits in rodents (e.g., Aggleton and Sahgal, 1993; Harding et al, 2000; Van der Werf et al, 2003; Tsivilis et al, 2008; Wolff et al, 2008; Vann, 2010; Carlesimo et al, 2011). These fornical interconnections have been of particular interest for understanding how fornix damage may disrupt memory in humans (Gaffan and Gaffan, 1991; Aggleton et al, 2000; Tsivilis et al, 2008), as well as in nonhuman primates and rats (e.g., Murray et al, 1989; Cassel et al, 1997; Bussey et al, 2000; Aggleton and Brown, 2002)

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