Synaptic feed-backs mediated by potassium ions.
Repetitive activity of the neuromuscular system and of neuronal centers leads to K+ efflux from excited cells and to its accumulation within extracellular spaces and synaptic clefts, especially during the generation of postsynaptic responses such as end-plate potentials or excitatory postsynaptic potentials. K+ ions accumulated within the synaptic cleft during activity modulate the transmitter secretion from motor nerve terminals. Depending on the concentration, K+ can either increase the transmitter release due to a specific presynaptic action or decrease it due to depolarization of the presynaptic membrane. The dual antidromic action of K+ can be the basis of functional self-regulation of the synapse. The significance of the positive presynaptic action of K+ can be assumed to enhance the reliability of the synaptic transmission at moderate activation rates. The negative presynaptic action of K+, which predominates at high-frequency activities or during neuromuscular fatigue, leads to randomized failures of transmissions at individual synapses, the overall pattern of activation of the entire system being reproduced. This might save the general capability of the system and protect its weakest elements. The positive antidromic action of K+ can be assumed to be essential to the mechanism of heterosynaptic facilitation and long-term potentiation at learning synapses of the brain.