The regulation of cyclic nucleotides in a sympathetic ganglion

Preganglionic nerve terminal stimulation in rat superior cervical ganglia causes marked increases in the levels of cyclic nucleotides. Results are similar when preganglionic nerve stimulation is compared with elevated [K+]0 or 4-aminopyridine. Although intact nerve terminals and Ca2+ are required for the response to occur, pharmacological studies indicate that acetylcholine and adrenergic transmitters are not involved in the cyclic nucleotide response. It is suggested that cyclic nucleotide accumulation occurs in the nerve terminals or an unknown transmitter or substance participates in the postsynaptic accumulation of the cyclic nucleotides. Polypeptides tested thus far do not seem to be implicated. Interrelationships among phospholipid turnover, Ca2+-exchange and cyclic nucleotide accumulation in rat sympathetic ganglia are considered, but are difficult to establish.