Intracellular alkalinization potentiates slow inward current and prolonged bursting in a molluscan neuron

The bilaterally paired ventral white cells (VWCs) of the buccal ganglion of Pleurobranchaea drive the cyclic motor output of ingestive feeding behavior during prolonged and endogenously sustained burst episodes. The capacity to support burst episodes is specifically induced by appetitive (food) stimulation of chemosensory pathways. Cyclic 3',5'-adenosine monophosphate (cAMP) and its agonists also induce prolonged burst episodes through potentiation of a slow inward current. Intracellular alkalinzation of the VWC by externally applied ammonium ion and methylamine (5-20 mM) induces bursting and enhances slow inward current measured under voltage-clamp conditions. The enhancement of slow inward current is seen in the induction or augmentation of a negative slope resistance region in the current-voltage relation and in the enhancement of slowly decaying inward current tails recorded near the K⁺ equilibrium potential following depolarizing voltage commands. Intracellular injection of alkalinizing agents, bicarbonate ion and a strong buffer solution at pH 8.1, also enhance the inward current. In ammonium saline, enhancement of inward current is dependent on NH₃ content, not NH⁺₄; NH₃ is the intracellular alkalinizing agent of ammonium saline. Therefore, the change in slow inward current is an effect specific to intracellular pH. The time courses of inward current enhancement and intracellular pH change in NH⁺₄ saline are similar. The results of this study suggest that normal fluctuations in intracellular pH may be significant determinants of the excitability and consequent activity of these and perhaps other neurons. The potential interaction of intracellular pH and cyclic AMP metabolism is discussed.