Arachidonic acid-activated membrane conductances in dissociated cardiac parasympathetic neurons from Necturus. Mulvaney, Jennifer M., and Rodney L. Parsons. Department of Anatomy and Neurobiology, University of Vermont, College of Medicine, Burlington, Vermont 05405, Phone: 802-656-2230, FAX: 802-656- 8704.
APStracts 2:0170N, 1995.
SUMMARY AND CONCLUSIONS
1. Characteristics of the membrane currents activated by arachidonic acid (AA) in dissociated mudpuppy parasympathetic neurons have been determined using the perforated patch whole cell recording technique. 2. In a sodium containing physiological solution with 12.5 mM potassium, AA (10 to 50 [mu]M) increased total membrane current produced by either depolarizing or hyperpolarizing voltage steps delivered from a holding potential of -40 mV. Decreasing the external potassium concentration from 12.5 mM to 2.5 mM shifted the reversal potential of the AA-induced current by 10 mV rather than the 42 mV predicted for a highly potassium selective channel. 3. In cells kept in sodium solution plus 12.5 mM potassium, and treated with 20 [mu]M nordihydroguaiaretic acid (NDGA), an inhibitor of the lipoxygenase pathway of AA metabolism, AA activated only inward currents following hyperpolarizing voltage steps. In this condition, the shift in reversal potential of the AA-induced current was 40 mV when extracellular potassium concentration was changed five-fold. Consequently, in cells treated with NDGA, AA appeared to activate only an inwardly rectifying potassium current. 4. Decreasing the extracellular chloride concentration by approximately 90% did not alter the reversal potential of the AA-activated current when the extracellular sodium concentration was kept constant and the external potassium concentration was 2.5 mM. In the low chloride solution, AA potentiated both inward and outward current amplitudes. These results suggested that AA did not activate a chloride current in these cells. 5. In a sodium-deficient, N-methyl-D- glucamine (NMG) containing solution, AA only activated currents for voltage steps to potentials more negative than the holding potential. In the NMG- substituted solution, changing the extracellular potassium concentration five- fold, shifted the reversal potential of the AA-induced current by 40 mV. Therefore, in the NMG solution, AA primarily activated an inwardly rectifying potassium current. 6. Exchanging the control solution containing AA to an external solution containing AA and barium (barium blocks the inwardly rectifying potassium current) shifted the I-V relationship to more positive voltages such that the extrapolated reversal potential was approximately 0 mV. In other experiments, using the barium containing solution, the reversal potential for the AA-induced current was -3.3 ¯+ 2.4 mV. 7. In conclusion, the results of the present study indicate that at least two membrane currents are activated in the presence of AA; an inwardly rectifying potassium current and an NDGA-sensitive, sodium dependent current which has a reversal potential more positive than the potassium equilibrium potential. We suggest the second current component is due to the activation of a non-selective cationic conductance. 

Received 9 January 1995; accepted in final form 18 May 1995.
APS Manuscript Number J17-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  8 June 1995.