Abstract
Adenosine depresses the excitability of pyramidal neurones in the hippocampus. This effect is lost in calcium-free media and we have now investigated the mechanism of this. Extracellular recordings were made of antidromically and orthodromically evoked population potentials from CA1 region of rat hippocampal slices. It was observed that the activity of adenosine can be restored in the presence of procaine or carbamazepine, known inhibitors of sodium channels. The GABA B agonist baclofen was able to depress potential size but did not restore sensitivity to adenosine. It is concluded that the loss of postsynaptic sensitivity to adenosine in calcium-free solution results from the increased sodium conductances.
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