NEURAL MECHANISMS OF BLOOD FLOW REGULATION DURING SYNAPTIC ACTIVITY IN
CEREBELLAR CORTEX.
Iadecola, Costantino, Jun Li, Sherry Xu and Guang Yang.
Laboratory of Cerebrovascular Biology and Stroke, Department of Neurology,
University of Minnesota Medical School, Minneapolis, MN 55455.
APStracts 2:0309N, 1995.
SUMMARY AND CONCLUSIONS
We investigated the neural mechanisms of the increases in blood flow produced
by synaptic activity using the parallel fiber (PF) system of the cerebellum as
a model. The midline cerebellum was exposed in anesthetized rats and the PF
were stimulated with tungsten microelectrodes. Cerebellar blood flow (BFcrb)
was recorded using a laser-Doppler probe whereas field potentials were
recorded using glass micropipettes. PF stimulation produced increases in BFcrb
that were related to the frequency and intensity of stimulation (+60+/-9% at
100 [mu]A and 30 Hz; n=6). The greatest increases were confined to a band
stretching along the major axis of the stimulated folium and corresponding to
the beam of activated PF. The increase in evoked by PF stimulation was
associated with a corresponding increase in glucose utilization, assessed by
the 2-deoxyglucose method. The increases in BFcrb and the field potentials
evoked by PF stimulation were abolished by tetrodotoxin (1 [mu]M; n=6). Ringer
containing 12 mM Mg ++ and 0 mM Ca ++ blocked synaptic activity in the PF and
abolished the increases in flow (p>0.05 from baseline; n=5). The broad
spectrum glutamate receptor antagonist kynurenate (5 mM) prevented
depolarization of Purkinje cells and interneurons and abolished the increase
in BFcrb evoked by PF stimulation (p>0.05; n=6). Treatment with tetrodotoxin,
Mg ++ or kynurenate did not affect the increase in BFcrb elicited by systemic
hypercapnia or by topical application of the nitric oxide donor 3-
morpholinosydnonimine (p>0.05 from Ringer). We conclude that the increases in
flow produced by synaptic activity are linked to glutamate-induced
depolarization of Purkinje cells and interneurons. These findings provide
evidence that activation of glutamate receptors participates in the mechanisms
of functional hyperemia and support the validity of the PF system as a model
to study the relationship between synaptic activity and blood flow in the
central nervous system.
Received 27 June 1995; accepted in final form 9 October 1995.
APS Manuscript Number J410-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95