Neurophysiology and pharmacology of long‐term potentiation in the rat sympathetic ganglion.

Abstract

Brief tetanic stimulation of the preganglionic nerve induced a persistent potentiation of nicotinic synaptic transmission in the rat superior cervical sympathetic ganglion. Quantitative measurements of the post-tetanic increase in synaptic efficacy revealed 2 distinct time courses. The early, rapidly decaying component, termed post-tetanic potentiation (PTP), had a decay time constant of 2-3 min. The duration of the most persistent component, called long-term potentiation (LTP), was extremely temperature dependent, lasting much longer at 32.degree. C than at 22.degree. C. In half of the experiments performed at 32.degree. C, LTP showed no detectable decay over the course of 1 h or more after a brief tetanic stimulation. Other experiments were conducted at 22.degree. C. The induction of LTP was dependent on the extracellular [Ca2+]. Transient elevation of the extracellular [K+] also produced a long-term enhancement of synaptic efficacy and this effect was Ca2+ dependent. The tetani that were effective in inducing LTP (5-20 Hz for 5-20 s) were well within the physiological range of preganglionic activity. The magnitude and time course were related to frequency and duration of stimulation. The occurrence of LTP was restricted to those preganglionic fibers that were tetanically stimulated. This lack of heterosynaptic or generalized effects was demonstrated by splitting the preganglionic nerve into 2 branches that could be independently tested and conditioned. Physiological activation of muscarinic or nicotinic receptors apparently does not play an essential role in causing ganglionic LTP, which is expressed as an enhancement of nicotinic transmission. A muscarinic antagonist (2 .mu.M-atropine) did not block LTP. Preganglionic stimulation induced LTP even when a high concentration of a nicotinic antagonist (3 mM-hexamethonium) was present during the tetanic stimulation. Bath application of a cholinergic agonist (100-1000 .mu.M-carbachol) could not substitute for tetanic stimulation in provoking LTP. Activation of adrenergic receptors does not play an essential role. Neither a .beta.-adrenergic antagonist (10 .mu.M-sotolol or 1 .mu.M propranolol) nor an .alpha.-adrenergic antagonist (1 .mu.M-phentolamine) had any significant effect on the magnitude or duration of LTP. Ganglionic LTP is a Ca2+- and temperature-dependent process that can be created independently of the activation of nicotinic, muscarinic or adrenergic receptors.