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Depolarization of isolated brain nerve endings by nitric oxide donors: membrane mechanisms.

Nitric oxide (NO) is known to potentiate neurotransmitter release in several types of neuronal cells. In the present study, the influence of NO on the membrane potential of isolated nerve endings (synaptosomes) from rat brain was studied. NO donors--sodium nitroprusside (SNP), S-nitroso-L-cysteine (CysNO), and hydroxylamine (HA)--induced synaptosome depolarization monitored by decreasing accumulation of 86Rb+ and the lipophilic potential-sensitive probe [3H]tetraphenylphosphonium. SNP reduced plasma membrane potential by 3-5 mV with half-maximal effect at approximately 10 microM. More potent NO donors, CysNO and HA, led to significant depolarization of the plasma membrane at 10-100 microM concentrations and also induced depolarization of mitochondria at concentrations above 1 mM. At 10 microM-10 mM concentrations, NO donors inhibited potassium channels; CysNO and HA also suppressed the activity of the sodium pump. NO-induced depolarization was not blocked by guanylate cyclase inhibitor methylene blue and the permeable cGMP analog dibutyryl-cGMP did not affect the membrane potential. The effects of NO donors were mimicked by SH-modifying reagents including 5, 5'-dithio-bis(2-nitrobenzoic acid) (DTNB) and N-ethylmaleimide (NEM). Non-permeable SH-reagent DTNB caused small depolarization resembling SNP action in its magnitude and kinetics. Significant decrease of potential in the presence of NEM, which permeates through the plasma membrane, was similar to that of CysNO and HA. The data suggest that in the presynaptic nerve endings, NO-induced depolarization of the plasma and mitochondrial membranes involves modification of protein SH-groups. The plasma membrane depolarization is due to the decreased potassium permeability and inhibition of the sodium pump.