Various acute brain pathological conditions are characterized by the presence of elevated glutamate
concentrations in the brain interstitial fluids. It has been established that a decrease in the blood glutamate
level enhances the brain-to-blood efflux of glutamate, removal of which from the brain may prevent glutamate
excitotoxicity and its contribution to the long-lasting neurological deficits seen in stroke. A decrease in blood
glutamate level can be achieved by exploiting the glutamate-scavenging properties of the blood-resident
enzyme glutamate-oxaloacetate transaminase, which transforms glutamate into 2-ketoglutarate in the
presence of the glutamate co-substrate oxaloacetate. The present study had the aim of an evaluation of the
effects of the blood glutamate scavenger oxaloacetate on the impaired long-term potentiation (LTP) induced in
the 2-vessel occlusion ischaemic model in rat. Transient (30-min) incomplete forebrain ischaemia was
produced 72 h before LTP induction. Although the short transient brain hypoperfusion did not induce
histologically identifiable injuries in the CA1 region (Fluoro-Jade B, S-100 and cresyl violet), it resulted in an
impaired LTP function in the hippocampal CA1 region without damaging the basal synaptic transmission
between the Schaffer collaterals and the pyramidal neurons. This impairment could be fended off in a dosedependent
manner by the intravenous administration of oxaloacetate in saline (at doses between 1.5 mmol and
0.1 μmol) immediately after the transient hypoperfusion. Our results suggest that oxaloacetate-mediated blood
and brain glutamate scavenging contributes to the restoration of the LTP after its impairment by brain
ischaemia