Zhu_1997_Neuropharmacol_36_169

The effects of endogenous adenosine release on CA1 neurons in hippocampal slices were studied under normoxic and hypoxic conditions, by using extra-/intracellular and whole-cell recordings. During normoxia, the adenosine antagonist, 8-(p-sulphophenyl) theophylline (8-SPT) or adenosine deaminase (ADA) potentiated both evoked CA1 EPSPs and spontaneous synaptic activity, but not monosynaptic IPSPs; there was a minimal depolarization (by 1 mV), probably caused by the enhanced synaptic activity, but no increase in input conductance. Under voltage-clamp with KCl electrodes (with holding potential (VH) near -70 mV), hypoxia (4-5 min) elicited a rise in input conductance and an outward current that reversed near -90 mV, in keeping with the activation of K conductance. These effects of hypoxia were partly attenuated by 8-SPT (10 microM). The hypoxia-induced outward current and conductance increase were abolished by 1 mM Ba, being replaced by a small inward current and a conductance decrease. These data indicate that adenosine tonically inhibits excitatory, but not inhibitory, synaptic transmission, has no direct effect on input conductance, and contributes to the hyperpolarization and fall in input resistance induced by hypoxia.