Sustained rise in ACh sensitivity of a sympathetic ganglion cell induced by postsynaptic electrical activities.

Long-term alteration in synaptic efficacy found in several neurones of both vertebrates and invertebrates has been suggested as an important mechanism for learning and memory. In bullfrog sympathetic ganglia, acetylcholine (ACh) release from presynaptic nerve terminals is potentiated for a long time by adrenaline through a cyclic AMP system. We report here a new form of mechanism for long-term synaptic potentiation in sympathetic ganglia, which occurs postsynaptically in a Ca2+-dependent manner. Our results suggest that Ca2+ entry into a ganglion cell during repeated action potentials initiates a long-lasting mechanism for the enhancement of a nicotinic ACh action on the subsynaptic membrane. This, as well as the presynaptic mechanism, may contribute to neuronal plasticity in the peripheral autonomic nervous system.