CEREBRAL-ISCHEMIA - ARE THE MEMORY DEFICITS ASSOCIATED WITH HIPPOCAMPAL CELL LOSS

Citation
J. Bachevalier et M. Meunier, CEREBRAL-ISCHEMIA - ARE THE MEMORY DEFICITS ASSOCIATED WITH HIPPOCAMPAL CELL LOSS, Hippocampus, 6(5), 1996, pp. 553-560
Citations number
85
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
10509631
Volume
6
Issue
5
Year of publication
1996
Pages
553 - 560
Database
ISI
SICI code
1050-9631(1996)6:5<553:C-ATMD>2.0.ZU;2-T
Abstract
The long-standing notion that damage restricted to the hippocampal for mation is sufficient to produce a significant global memory deficit de rives from clinical data. Specifically, it is based on the observation that transient global ischemia, which leads to partial cell loss with in the hippocampal formation but not in other brain areas important fo r memory, can produce global amnesia in humans. This view is, however, challenged by a number of experimental findings. First, in both monke ys and rats, there is evidence that ischemia disrupts delayed object r ecognition, a memory process found to be largely intact following sele ctive hippocampal lesions. These findings indicate that damage confine d to the hippocampal formation cannot account for all aspects of the i schemia-induced memory impairments. Second, although some groups of hi ppocampal neurons are the most prone to degeneration following ischemi a, a wide array of extra-hippocampal damage has been observed in all s pecies, for which the precise extent and distribution may well be unde restimated by conventional histological evaluations of ischemic brains . Partial neuronal degeneration reported in regions such as the rhinal areas, medial dorsal thalamic nucleus, or cingulate cortex may contri bute to varying degrees to ischemia-induced memory deficits. Third, ex perimental studies have failed to generate a general consensus on the correlation between extent of hippocampal cell loss and memory perform ance. In sum, the experimental studies do not, as yet, support the vie w that hippocampal damage is solely responsible for ischemia-induced m emory deficits. Rather, they suggest that both the intra- and extra-hi ppocampal damage contribute to the pattern of memory impairments obser ved following ischemia. Consequently, although animals with global and focal ischemia represent valuable models for neuropathological and th erapeutic studies, they may not be so useful in assessing the role of the hippocampal formation and its sub-components in memory processes. (C) 1996 Wiley-Liss, Inc.