Synaptic plasticity is a term that describes long-lasting changes in the efficacy of synaptic transmission resulting from certain patterned activities of the presynaptic nerve. One form of synaptic plasticity, long-term potentiation (LTP), is an activity-dependent marked increase in synaptic efficacy that has been extensively studied in various regions of the central nervous system, particularly the hippocampus, where LTP is widely believed to be a cellular correlate of learning and memory. A similar phenomenon has been identified in sympathetic ganglia even before Bliss and Lomo coined the term LTP in 1973. Ganglionic LTP (gLTP) of the nicotinic pathway is a similarly long-lasting increase in synaptic effectiveness that can be induced in ganglia following a brief train of relatively high frequency stimulation (HFS) of the preganglionic nerve. Remarkably similar to the LTP of the hippocampus, gLTP has been demonstrated in autonomic ganglia from a number of vertebrates including mammalian, amphibian and avian species. Several other forms of long-lasting increases in synaptic effectiveness have been demonstrated in sympathetic ganglia following exposure to adrenergic agonists, neuroactive peptides and cyclic nucleotides and even after a challenge by an antigen. The main emphasis of this review, however, will be on the activity-dependent gLTP of the mammalian sympathetic ganglia, in particular the superior cervical ganglion of the rat. Since the last, excellent and comprehensive review of this ganglionic function by Briggs in 1995, important discoveries about the mechanisms of induction and maintenance of gLTP have been reported, including the finding that the response is uniquely dependent on serotonin for both the induction phase and maintenance phase. These new advances will be discussed in depth in this review.