The presynaptic effects of arachidonic acid and prostaglandin E2 at the frog neuromuscular junction.

Arachidonic acid and prostaglandin E2 decreased the frequency of miniature endplate potentials with producing any changes in the their amplitude-time parameters. Arachidonic acid and prostaglandin E2 decreased the quantum composition of endplate currents and the amplitude of the third phase of the nerve ending response, which reflects currents though potential-dependent K+ channels. A perineural method was used to demonstrate that arachidonic acid and prostaglandin E2 suppressed the nerve ending Ca2+ current. The cyclooxygenase blocker indomethacin increased neurotransmitter secretion and decreased the third phase of the nerve ending response. The effects of arachidonic acid and prostaglandin E2 on evoked neurotransmitter release were not seen in the presence of indomethacin, while the third phase of the response continued to show a reduction. It is suggested that prostaglandin E2 mediates the effects of arachidonic acid on spontaneous and evoked neurotransmitter secretion, Ca2+ currents, and Ca2+ -dependent K+ currents. In addition, arachidonic acid and prostaglandin E2 had their own effects on potential-dependent K+ currents in nerve endings.