Differential effect of adenosine on pre- and postsynaptic calcium fluxes.
In rat hippocampal slices, stimulus-evoked field potentials and the concomitant decrease of the extracellular concentration of free Ca ions [Ca2+]o were measured with combined reference/ion-sensitive microelectrodes. By reducing [Ca2+]o from 2.0 mM to 0.2 mM, evoked synaptic transmission was blocked, but orthodromic repetitive stimulation of CA1 afferents still elicited a marked decrease of [Ca2+]o. This Ca2+ signal is attributed predominantly to Ca2+ entry into the activated axon terminals. It was significantly depressed by adenosine. The adenosine agonist, L-phenylisopropyl adenosine (L-PIA) was more effective than D-PIA, indicating that the adenosine depression of presynaptic Ca2+ entry is mediated via the A1 receptor. 4-Aminopyridine (4-AP) enhanced decreases in [Ca2+]o without restoring synaptic transmission. Adenosine depressed also these Ca2+ signals. Adenosine deaminase was even more effective in the presence of 4-AP and enhanced the orthodromic Ca2+-signal by a factor of two. Antidromic stimulation of hippocampal pyramidal cells also evoked reductions in [Ca2+]o. These were less affected by adenosine and the other treatments under the conditions tested.
D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002463:Cell Membrane Permeability / Q000187:drug effects; D005071:Evoked Potentials / Q000187:drug effects; D006624:Hippocampus / Q000378:metabolism*; D066298:In Vitro Techniques; D051381:Rats; D013570:Synaptic Membranes / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects*
D000241:Adenosine; D002118:Calcium