J. Nunn et H. Hodges, COGNITIVE DEFICITS INDUCED BY GLOBAL CEREBRAL-ISCHEMIA - RELATIONSHIPTO BRAIN-DAMAGE AND REVERSAL BY TRANSPLANTS, Behavioural brain research, 65(1), 1994, pp. 1-31
The CA1 and hilar fields of the hippocampus are highly vulnerable to l
ack of oxygen after interruption of blood flow to the brain. Severe an
terograde memory loss, seen in a significant proportion of heart attac
k survivors, has been attributed to selective bilateral ischaemic dama
ge to the hippocampus. Animal models of global ischaemia, induced by e
xtracranial occlusion of the major ascending arteries, enable assessme
nt of the neuropathological and functional consequences of transient i
nterruption of cerebral blood flow, and can inform strategies to reduc
e or alleviate ischaemic brain damage. This review focuses firstly on
the nature of cognitive deficits induced by global ischaemia, how far
they are consistent with lesion-based accounts of hippocampal function
, and the extent to which these deficits can be correlated with CA1 ce
ll loss. The second focus of the review is to examine the limited evid
ence for graft-induced recovery of cognitive function in animals subje
cted to global ischaemia. Recent findings that grafted foetal cells fr
om discrete hippocampal fields follow appropriate laminar routes to fo
rm functional connections with host neurons, and that growth factors p
rotect cells from ischaemic damage, have suggested that CA1 or trophic
grafts placed in the region of ischaemic CA1 cell loss might restore
or protect this vulnerable sector, and reduce cognitive deficits.