PURINERGIC INHIBITION OF GABA AND GLUTAMATE RELEASE IN THE THALAMUS -IMPLICATIONS FOR THALAMIC NETWORK ACTIVITY

Adenosine is a CNS depressant with both pre- and postsynaptic actions. Presynaptically, adenosine decreases neurotransmitter release in the hippocampus but only at excitatory terminals. In the thalamus, however , we show that, in addition to its actions at excitatory synapses, ade nosine strongly supresses monosynaptic inhibitory currents both in rel ay cells of the thalamic ventrobasal complex (VB) and in inhibitory ne urons of the nucleus reticularis thalami (nRt). A concomitant increase in transmission failures and results coefficient of variation analysi s are both consistent with a presynaptic mechanism. Pharmacological ma nipulations support an A1 receptor-mediated process. Slow thalamic osc illations induced in vitro by extracellular stimulation and recorded w ith extracellular multiunit electrodes in VB and nRt are dampened by a denosine without affecting their periodicity. We conclude that adenosi ne can presynaptically downregulate inhibitory postsynaptic responses in thalamus and exert robust antioscillatory effects, likely by synerg istic depression of both excitatory and inhibitory neurotransmitter re lease.