The Receptor‐Mediated Activation of Tyrosine Hydroxylation in the Superior Cervical Ganglion of the Rat

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Abstract
The addition of carbachol to superior cervical ganglia causes a rapid increase in tyrosine hydroxylation in situ. The increase occurs in ganglia from both newborn and adult animals, and in ganglia from animals pretreated with reserpine. The increase is not due to increased transport of the substrate. The increase is dependent upon the presence of Ca, and is additive to the stimulation produced by dibutyryl cAMP. The stimulation seems specific for tyrosine hydroxylation; dopamine .beta.-hydroxylation is not increased. Preincubation experiments suggest that the carbachol-induced stimulation is due to a change in the availability of, or the affinity of the enzyme for, reduced pterin cofactor. The stimulation is inhibited by atropine and also by low concentrations of phenoxybenzamine or haloperidol, which suggests that it is caused by an action of carbachol on the interneurons in the ganglia.