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Hippocampal lesions halve immediate-early gene protein counts in retrosplenial cortex: distal dysfunctions in a spatial memory system

Albasser, Mathieu M., Poirier, Guillaume L., Warburton, E. Clea and Aggleton, John Patrick 2007. Hippocampal lesions halve immediate-early gene protein counts in retrosplenial cortex: distal dysfunctions in a spatial memory system. European Journal of Neuroscience 26 (5) , pp. 1254-1266. 10.1111/j.1460-9568.2007.05753.x

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Abstract

The present study examined whether hippocampal lesions disrupt retrosplenial cortex function. The immediate–early genesc-fos and zif268 provided markers of cellular activity, and their levels were compared in different cytoarchitectonic subregions (dysgranular, granular a and granular b) and different layers (superficial or deep) within retrosplenial cortex. Experiments 1–3 examined the impact of hippocampal lesions on retrosplenial cortex function, with the variations in protocol (e.g. lesion method, rat strain, behaviour prior to gene activity measurement) testing the generality of the findings. Experiment 1 showed that radio-frequency hippocampus lesions result in very striking losses of Fos and Zif268 activity in both superficial and deep laminae of all retrosplenial subregions. This pattern of results was repeated for Fos in experiments 2 and 3. Despite the loss of Fos and Zif268, there was no evidence of retrosplenial cortex atrophy as measured by Nissl counts (experiments 1–3) or NeuN-positive cell counts (experiment 3). Likewise, there was little evidence of any overt changes in cellular size, shape or appearance. The specificity of these hippocampal lesion effects was confirmed in experiment 4 as entorhinal cortex lesions did not change retrosplenial Fos levels. These results provide strong support for the notion that the retrosplenial cortex is unusually sensitive to deafferentation from some of its inputs, so that hippocampal damage might produce permanent ‘covert pathology’ in the retrosplenial cortex. Such dysfunctions could contribute to the pattern of cognitive changes associated with hippocampal lesions and also help to explain the functional interdependency of these two structures.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Psychology
Medicine
Neuroscience and Mental Health Research Institute (NMHRI)
Subjects: R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Uncontrolled Keywords: c-fos; entorhinal cortex; hippocampus; rat; zif268
Publisher: Wiley-Blackwell
ISSN: 0953-816X
Last Modified: 04 Jun 2017 02:42
URI: http://orca.cf.ac.uk/id/eprint/11359

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