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Role of arachidonic acid in depolarization-induced modulation of ion currents in Aplysia giant neurons.

1. The effects of membrane depolarization on inward currents subsequently elicited by hyperpolarization were studied with the use of two-electrode, voltage-clamp techniques in the giant neurons LP1 and R2 of Aplysia. 2. Several successive sets of brief depolarizing pulses, or bursts, were used to depolarize the giant neurons. Two distinct inward currents elicited by hyperpolarization were found to be altered after these sets of depolarizing pulses. These currents were distinguished by their voltage dependence, reversal potential, and sensitivity to 1 mM BaCl2. One of the inward currents was increased after depolarization. It was outwardly rectifying, reversed at -50 mV, and not blocked by Ba2+, suggesting it was a chloride current (ICl). The other inward current, which was decreased after depolarization, was inwardly rectifying, reversed at -70 mV, and completely inhibited by Ba2+. These are characteristics of the inwardly rectifying potassium current (IR), a current previously described to be inhibited after depolarization in Aplysia neuron R 15. Depolarization typically increased the putative ICl and decreased IR for minutes, with the decrease in IR consistently outlasting the increase in an initial brief net increase in inward current followed by a long-lasting decrease. 3. Several criteria suggest arachidonic acid (AA) may mediate depolarization-induced modulation of IR. Previously, free AA has been shown to constitutively inhibit IR in the resting state. Also, depolarization has been reported to stimulate liberation of AA from storage in Aplysia ganglia. Consistent with previous results in neuron R 15, depolarization-induced modulation of IR in giant neurons was dependent on external calcium. Indomethacin and 4-bromophenacylbromide (BPB), pharmacologic agents that activate IR through inhibition of AA turnover, altered the effect of depolarization on IR. In contrast serotonin (5HT), which activates IR through adenosine 3',5'-cyclic monophosphate (cAMP), did not alter the effect of depolarization. Also, extended perfusion with bovine serum albumin (BSA), which strips AA from lipid storage in neurons, decreased the depolarization-induced modulation of IR. We conclude that the calcium influx accompanying depolarization activates the phospholipase responsible for liberation of AA from phospholipid, and the liberated AA then acts to inhibit IR. The molecular mechanism of this AA-mediated inhibition remains to be determined. 4. Depolarization-induced modulation of ICl was also dependent on external calcium but was not affected by BPB and only slightly decreased with indomethacin. This suggested AA was probably not involved in this modulation. However, 5HT opposed the modulation of IC1 induced by previous depolarization, suggesting cAMP may be involved in this effect of depolarization.