Intracellular sodium accumulation and transmitter release at crustacean neuromuscular junctions.

Since the intracellular concentrations of Na+ and Ca2+ are relatively low and the cell's ability to actively expel or sequester these ions is limited, prolonged, high-frequency impulse activity at many crustacean axon terminals can result in significant increases in [Na+]i and [Ca2+]i. These changes parallel increases in transmitter output and may persist for several seconds (short-term facilitation, or STF) or even for many hours (long-term facilitations, or LTF). These two phenomena appear to be qualitatively distinct processes. The unique properties of LTF include: 1) the need for Na+ (but not Ca2+) in the extracellular media; 2) long decay times (from minutes to hours); 3) acceleration of devolpment and retardation of decay under conditions that inhibit the membrane Na+-K+ pump, e.g., cardiac glycosides, low [K+]o. The subcellular mechanism(s) linking Na+ accumulation to increased transmitter release are unknown but may involve alterations in [Ca2+]i, either through release from intracellular stores or through increased membrane conductance. Sodium-induced modifications in transmitter synthesis, storage, or availability may also be involved. Long-term functional changes in synaptic efficacy like LTF may provide important clues to more general questions of nervous system plasticity.