Stimulation of the synthesis of catecholamines in a sympathetic ganglion via cholinergic and non-cholinergic mechanisms.

Electrical stimulation of the preganglionic sympathetic neurons rapidly and markedly elevated the contents of the primary dopamine (DA) and noradrenaline (NA) metabolites, i.e., 3,4-dihydroxyphenylacetic acid (DOPAC) and 3,4-dihydroxyphenylethylene glycol (DOPEG) in the superior cervical ganglion and it enhanced the accumulation of DOPAC and DA following inhibition of the DA-beta-hydroxylase by FLA-63. The stimulation also increased the concentration of DA and decreased the concentration of NA in the salivary gland both without and with DA-beta-hydroxylase inhibition. Chlorisondamine inhibited the increase in ganglionic DOPAC following preganglionic stimulation (5 Hz, 30 min) by 30-50% and it even better reduced the biochemical changes in the salivary gland. Atropine did not produce any clearcut inhibition of the stimulation-induced effects on the superior cervical ganglion or the salivary gland, nor did it enhance the effect of chlorisondamine. The results suggest that nicotine, but not muscarine receptors in the cell body region of the postganglionic NA neurons partially mediate the effects of preganglionic stimulation. The effects remaining after blockade of the nicotine and muscarine receptors might be due to release of a neuropeptide acting on a special receptor. The stimulation-induced increase in the concentration of DOPAC in the superior cervical ganglion might, at least partly, be the result of a depolarization of the NA nerve cell body regions since similar changes were produced by electrical stimulation of the chronically decentralized ganglion.