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The effect of NH4+ on synaptosomal membrane potential was examined using rat brains. The membrane potential was measured by the rhodamine 6G fluorescence method. Both NH4+ diffusion potential (NH4+-potential) and K+ diffusion potential (K+-potential) were observed in the synaptosomes. Upon replacement of medium Cl- with SCN-, both K+- and NH4+-potentials depolarized. On the other hand, replacement of medium Cl- with gluconate resulted in the hyperpolarization of K+-potential, but not of NH4+-potential. Ethacrynic acid (0.3 mM), a Cl- -ATPase inhibitor, depolarized both K+(Cl-)- and NH4+ (Cl-)-potentials. In the presence of ethacrynic acid, both of the potentials were further depolarized by replacement of medium Cl- with SCN-, but not with gluconate-. Picrotoxin (5 mM), a Cl- channel inhibitor, did not significantly affect either K+- or NH4+-potential. In the presence of picrotoxin, replacement of medium Cl- with SCN- depolarized both K+- and NH4+-potentials with or without ethacrynic acid. Gluconate depolarized the K+-potential with ethacrynic acid and the NH4+-potential with or without ethacrynic acid. These findings suggest that NH4+ forms a diffusion potential in nerve endings, and inhibits the anion-mediated hyperpolarization through mechanisms other than anion channels.

Effect of NH4+ on synaptosomal membrane potential in the rat brain.