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Vol. 293, Issue 1, 172-179, April 2000
Department of Anatomy and Cell Biology, Queen's University,
Kingston, Ontario, Canada
It has been proposed that extracellular ATP inhibits synaptic
release of glutamate from hippocampal CA1 synapses after its catabolism
to adenosine. We investigated the possibility that at least part of
this effect is mediated by ATP itself acting on P2Y receptors. ATP and
various analogs decreased the amplitude and duration of
glutamate-mediated excitatory postsynaptic potentials in all tested
neurons. This effect was reversible and concentration-dependent and had
the following rank order of agonist potency: AMP = ATP = adenosine-5'-O-(3-thio)triphosphate > adenosine = ADP. 
,
-Methylene ATP, ,
-methylene ATP,
2-methylthioadenosine 5'-triphosphate, GTP, and UTP induced only a
partial response. The depolarization induced by exogenous glutamate was
not affected by ATP, indicating that this nucleotide acts
presynaptically to inhibit glutamate-mediated excitatory postsynaptic
potentials. Neither inhibition of ectonucleotidase activity with
,-methylene ADP, suramin, or
pyridaxalphosphate-6-azophenyl-2',4'-disulfonic acid 4-sodium nor
removal of extracellular adenosine (with adenosine deaminase) altered
ATP effects. 8-Cyclopentyltheophylline competitively inhibited ATP
effects, whereas P2 receptor antagonists
(pyridaxalphosphate-6-azophenyl-2',4'-disulfonic acid 4-sodium,
suramin, and reactive blue 2) were ineffective. ATP effects were by far
more sensitive to pertussis toxin (PTX) than those of adenosine. After
PTX, adenosine-5'-O-(3-thio)triphosphate induced only a
partial response, and ATP concentration-response curve was biphasic.
The second phase of this curve was blocked by adenosine deaminase,
implying that it is mediated by adenosine as a result of ATP
catabolism. Under control conditions, however, catabolism of ATP is not
required to explain its actions. In conclusion, ATP inhibits synaptic
release of glutamate by direct activation of P2Y receptors that are
PTX- and 8-cyclopentyltheophylline-sensitive.
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