The effect of corticoids (hydrocortisone and dexamethasone) and epinephrine on the presynaptic action of purines was studied at the neuromuscular junction of the frog under two-electrode voltage-clamp conditions. Daily administration of hydrocortisone/dexamethasone (100 mg/kg into the lymphatic system) increased initially and depressed later on the amplitude of ultiquantum end-plate currents evoked by motor nerve stimulation. An initial facilitatory phase of the hormone action was accompanied by removal of the presynaptic action of ATP (for hydrocortisone only). Within the later phase (2 weeks of hydrocortisone administration), the inhibitory action of ATP was restored once again. Counteraction of ATP effect was reproduced under superfusion of the isolated muscle by a physiological solution containing hydrocortisone (not dexamethasone), indicating a non-genomic nature of the action of hormone onto presynaptic P2 receptors. It proved to be true by experiments on animals, which were stressed 30 min prior to the beginning of the experiment by electrical stimulation in a special cage. Independently of acute or chronic administration of hydrocortisone, the presynaptic action of another purine, adenosine, remained preserved. Epinephrine only partially abolished the inhibitory effect of purines, that is indicative of a difference in the paths of incorporation for biological effects of these agents. We suggest that prevention of an inhibitory action of ATP might be one of the components of a facilitatory acute stress reaction, while such an inhibitory feedback action is missing under chronic stress conditions.

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