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The Receptor‐Mediated Activation of Tyrosine Hydroxylation in the Superior Cervical Ganglion of the Rat
Author(s) -
Ikeno Takeyuki,
Dickens Geneva,
Lloyd Tom,
Guroff Gordon
Publication year - 1981
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1981.tb00413.x
Subject(s) - stimulation , reserpine , medicine , endocrinology , hydroxylation , carbachol , superior cervical ganglion , phenoxybenzamine , chemistry , haloperidol , tyrosine hydroxylase , tyrosine , dopamine , biology , receptor , biochemistry , enzyme
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 calcium, and is additive to the stimulation produced by dibutyryl cyclic AMP. The stimulation seems specific for tyrosine hydroxylation; dopamine β‐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.