Synaptosomal calcium uptake unaltered by adenosine and 2-chloroadenosine.

Purinergic compounds can decrease neural activity peripherally and centrally [l-4]. The spontaneous firing rates of cerebellar Purkinje neurons fall precipitously after adenosine or its analogs are applied locally [5]. The amplitude of hippocampal excitatory postsynaptic potential (EPSP) responses is depressed by adenosine and its analogs [S, 61. The depression of EPSP amplitudes of pyramidal neurons of the hippocampus is unaccompanied by changes of resting membrane potential or resistance following perfusion with 5 PM adenosine, implying presynaptic effects, but treatment with 10pM adenosine produces a hyperpolarization with a reduction of input resistance [6]. Hyperpolarization without a change of resistance has been reported for cerebral cortical neurons after iontophoresis of adenosine 5’-monophosphate (71. Neurotransmitter release is decreased by purinergic compounds, Adenosine (0.01 mM) reduces the depolarizationinduced release of dopamine, acetylcholine and 5-hydroxytryptamine from striatal slices [8]. Adenosine triphosphate (0.1 to 0.5mM) inhibits the release of acetylcholine, as shown by decreased synaptic responses of sympathetic ganglion cells, but adenosine (0.4 to 0.75 mM) is without effect on these responses 191. Adenosine is suggested to reduce neurotransmitter release by blockade of calcium channels [Z]. The suggestion of calcium involvement in the reduction of transmitter release is based upon reports of adenosineinduced inhibition of calcium uptake by synaptosomes [lo, 111. To further evaluate this possibility of presynaptic calcium mechanisms, we examined the effects of adenosine and 2-chloroadenosine on fastand slow-phase voltagedependent calcium entry into synaptosomes.