scholarly journals Neural systems underlying episodic memory: insights from animal research

2001 ◽  
Vol 356 (1413) ◽  
pp. 1467-1482 ◽  
Author(s):  
John P. Aggleton ◽  
John M. Pearce

Two strategies used to uncover neural systems for episodic–like memory in animals are discussed: (i) an attribute of episodic memory ( what ? when ? where ?) is examined in order to reveal the neuronal interactions supporting that component of memory; and (ii) the connections of a structure thought to be central to episodic memory in humans are studied at a level of detail not feasible in humans. By focusing on spatial memory ( where ?) and the hippocampus, it has proved possible to bring the strategies together. A review of lesion, disconnection and immediate early–gene studies in animals reveals the importance of interactions between the hippocampus and specific nuclei in the diencephalon (most notably the anterior thalamic nuclei) for spatial memory. Other parts of this extended hippocampal system include the mammillary bodies and the posterior cingulate (retrosplenial) cortex. Furthermore, by combining lesion and immediate early–gene studies it is possible to show how the loss of one component structure or tract can influence the remaining regions in this group of structures. The validity of this convergent approach is supported by new findings showing that the same set of regions is implicated in anterograde amnesia in humans.

2018 ◽  
Vol 2 ◽  
pp. 239821281881123 ◽  
Author(s):  
Anna L Powell ◽  
Emma Hindley ◽  
Andrew JD Nelson ◽  
Moira Davies ◽  
Eman Amin ◽  
...  

The retrosplenial cortex forms part of a network of cortical and subcortical structures that have particular importance for spatial learning and navigation in rodents. This study examined how retrosplenial lesions affect activity in this network by visualising the expression of the immediate-early genes c- fos and zif268 after exposure to a novel location. Groups of rats with extensive cytotoxic lesions (areas 29 and 30) and rats with lesions largely confined to area 30 (dysgranular cortex) were compared with their respective control animals for levels of c- fos expression measured by immunohistochemistry. These cortical lesions had very limited effects on distal c- fos activity. Evidence of a restricted reduction in c-fos activity was seen in the septal dentate gyrus (superior blade) but not in other hippocampal and parahippocampal subareas, nor in the anterior cingulate and prelimbic cortices. Related studies examined zif268 activity in those cases with combined area 29 and 30 lesions. The only clear evidence for reduced zif268 activity following retrosplenial cell loss came from the septal CA3 area. The confined impact of retrosplenial tissue loss is notable as, by the same immediate-early gene measures, retrosplenial cortex is itself highly sensitive to damage in related limbic areas, showing a marked c- fos and zif268 hypoactivity across all of its subareas. This asymmetry in covert pathology may help to explain the apparent disparity between the severity of learning deficits after retrosplenial cortex lesions and after lesions in either the hippocampus or the anterior thalamic nuclei.


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