The action of cAMP and catecholamines in mammalian sympathetic ganglia.

Electrophysiological approaches using intracellular microelectrode techniques have failed to critically test the hypothesis that cyclic AMP (cAMP) mediates the slow inhibitory postsynpatic potential (IPSP). The slow IPSP is not readily elicited, and the resting membrane potential is relatively insensitive to application of catecholamines and adenine nucleotides. However, comprehensive studies of voltage-dependent events in postganglionic neurons reveal three Ca2+-dependent potentials that are quite sensitive to catecholamines and adenine nucleotides. The hyperpolarizing afterpotential, the action potential shoulder, and the Ca2+ spike are all inhibited by alpha-adrenergic agonists, adenosine, and cAMP. We have proposed that simulation of alpha-adrenergic and adenosine receptors on the post-synaptic membrane results in antagonism of an inward Ca2+ current. Further experimentation is necessary to determine if cAMO acts as a second messenger or only by activating an adenosine receptor. Preliminary studies suggest that catecholamines and adenine nucleotides have similar and potent actions on the terminals of preganglionic axons. Here, inhibition of Ca2+ influx results in reduced acetylcholine release but facilitates high-frequency cholinergic transmission. More quantitative biophysical and pharmacological studies are required to better characterize the synaptic mechanisms in sympathetic ganglia.