Adenosine action on interneurons and synaptic transmission onto interneurons in rat hippocampus in vitro
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abstract
To investigate the action of adenosine on interneurons as well as on excitatory synaptic transmission onto interneurons in the hippocampus, intracellular recordings were made from electrophysiologically identified interneurons in the CA1 region of the hippocampal slice in vitro. The effects of adenosine and the preferential adenosine A1 receptor agonist, chloroadenosine, were examined. Application of 50 microM adenosine and 20 microM chloroadenosine to the bath produced a hyperpolarization of 5.6+/-1.6 (n=5) and 6.1+/-1.4 mV (n=6), respectively, as well as a decrease in membrane input resistance of 18.1+/-3.5% (n=5) and 18.5+/-1.4% (n=6), respectively. Adenosine depressed the postsynaptic potentials (PSPs) elicited in the interneurons by stimulation of Schaffer collateral fibers by 73+/-6.8% (n=5). The amplitude and the duration of the afterhyperpolarization which followed the spike of the action potential were attenuated by 48+/-6.9% and 31+/-8.6%, respectively (n=5). Chloroadenosine depressed the evoked PSPs in these interneurons by 61.2+/-2.7% (n=6) and depressed the duration and the amplitude of the afterhyperpolarization by 85.2+/-4.5% and by 72.6+/-4.8%, respectively (n=6). The data show that adenosine and chloroadenosine directly inhibit hippocampal CA1 interneurons by blocking the synaptic input, by hyperpolarizing the membrane potential and by depressing the afterhyperpolarization following individual action potential spikes. It is proposed that adenosine A1 receptors are present at pre- and/or postsynaptic sites of interneuron synapses in the hippocampal CA1 region. The present findings demonstrate that adenosine A1 receptor activation in CA1 interneurons is able to modulate the excitatory synaptic input to, and excitability of, these neurons. Thus, as adenosine is released during ischemia and epilepsy, adenosine may protect both interneurons and pyramidal cells from glutamate excitotoxicity through activation of adenosine A1 receptors on these neurons in the hippocampus.
