Chronic reductions in cerebral blood flow (CBF) of between 25 and 50%, in t
he absence of cerebral infarction, lead to impairments in hippocampal in vi
tro long-term potentiation (LTP), This study set out to explore some of the
properties of this impairment of LTP. LTP is an electrophysiological prope
rty known to occur in the hippocampus, a region known to be exquisitely sen
sitive to hypoxic or ischemic insults. Thus, assessing LTP is a novel way o
f assessing the effects of subtle ischemic;insults, Five male Sprague-Dawle
y rats had arteriovenous fistulae created surgically in the neck to induce
a state of chronic cerebral hypoperfusion (CCH) with the features described
above. Five rats were used as ape-matched controls. Twenty-six weeks after
fistula formation, the animals were prepared for in vitro hippocampal reco
rding in a submerged tissue bath. Extracellular field potentials were recor
ded at the Schaffer collateral-CA1 region, with a stimulus intensity that a
chieved a population spike amplitude of 1 mV. After tetanic stimulation, th
e frequency and magnitude of LTP was compared between control and fistula a
nimals, All animals in both these groups demonstrated LTP in contradistinct
ion to our previous work where LTP was impaired in fistula animals when a h
igher intensity of stimulation was used. This indicates that the structures
that are associated with the initiation and maintenance of LTP (most proba
bly the ischemia-sensitive CAI pyramidal cells) are saturated as the stimul
us intensity is increased. Thus, at this lower intensity of stimulation LTP
is preserved in the fistula animals, but found to be impaired as the stimu
lus intensity is increased, Consequently, this study provides further infor
mation on this newly identified subtype of chronic cerebral ischemia which:
in time, after further studies in humans, may help to redefine therapeutic
indicators for the management of cerebral arteriovenous malformation and s
evere cerebrovascular disease.