The hypothesis that release of adenosine following spinal cord injury (SCI)
may provide neuroprotective feedback is explored. Consistent with this hyp
othesis, substantial release of adenosine, estimated to reach 100 mu M in t
he extracellular space, was detected by microdialysis sampling immediately
following contusion SCI. There is also considerable release of excitatory a
mino acids following SCI. The latter was not affected by administration of
the general adenosine receptor antagonist theophylline and the A, antagonis
t 8-cyclopentyl-1,3-dipropylxanthine, implying that the adenosine released
following SCI does not significantly influence the release of neurotoxic am
ino acids. Administration of the concentration of glutamate released upon S
CI into the spinal cord caused only about 1% as much release of adenosine a
s did injury, evidence that elevated excitatory amino acids do not elicit a
n appreciable fraction of the release of adenosine that follows SCI. Result
s obtained suggest that release of endogenous adenosine is not neuroprotect
ive by blocking release of excitatory amino acids following SCI. (C) 2000 E
lsevier Science B.V. All rights reserved.