Abstract
ADENOSINE is postulated to function in the brain as an inter-cellularly active neurohumoral substance. This has been suggested by in vitro studies showing that adenosine can be released from brain tissue by electrical stimulation at quantities which are sufficient to increase the formation of cyclic AMP1. The finding that adenosine derivatives are released from dendrites and particularly axon terminals points to the neurones as a major source for the released nucleotides2. Thus, nucleotides may function as ‘secondary’ or ‘additional’ neuronal transmitters mediating long lasting effects of a neurone on the metabolism and function of its target cells. Further evaluation of these hypotheses will require demonstrations that endogenous adenosine or its derivatives are actually released by synaptic connections in the intact brain and that this process is influenced by activation of these connections. We have carried out experiments in which tritiated adenosine was transported from cell bodies into a population of terminals, and in which the amount of radioactive materials taken up by the target cells of these terminals was measured in the presence and absence of synaptic stimulation. Stimulation was found to increase the release of 3H-adenosine derivatives from central axon terminals to their postsynaptic neurones.
Published Version
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