Enhancement by choline of the induction of adrenal tyrosine hydroxylase by phenoxybenzamine, 6-hydroxydopamine, insulin or exposure to cold.
Treatments that increase the release of acetylcholine from the splanchnic nerve have previously been shown to induce the enzyme tyrosine hydroxylase in adrenal chromaffin cells. Such treatments include the systemic administration of the drugs phenoxybenzamine and 6-hydroxydopamine, insulin-induced hypoglycemia, and prolonged exposure to cold. We have reported that the administration of choline also induces the adrenal enzyme and have suggested that the mechanism of this induction involves an increase in the amount of acetylcholine released each time the splanchnic nerve fires. In the present studies, rats received both choline and one of the above treatments. Choline caused an augmentation of the adrenomedullary response to each of the treatments, but it had no apparent effect on a presynaptic enzyme, choline acetyltransferase. These observations strongly support the view that choline availability determines both the amount of acetylcholine present in nerve terminals and the amount liberated when cholinergic neurons fire.
Enhancement by choline of the induction of adrenal tyrosine hydroxylase by phenoxybenzamine, 6-hydroxydopamine, insulin or exposure to cold. Treatments that increase the release of acetylcholine from the splanchnic nerve have previously been shown to induce the enzyme tyrosine hydroxylase in adrenal chromaffin cells. Such treatments include the systemic administration of the drugs phenoxybenzamine and 6-hydroxydopamine, insulin-induced hypoglycemia, and prolonged exposure to cold. We have reported that the administration of choline also induces the adrenal enzyme and have suggested that the mechanism of this induction involves an increase in the amount of acetylcholine released each time the splanchnic nerve fires. In the present studies, rats received both choline and one of the above treatments. Choline caused an augmentation of the adrenomedullary response to each of the treatments, but it had no apparent effect on a presynaptic enzyme, choline acetyltransferase. These observations strongly support the view that choline availability determines both the amount of acetylcholine present in nerve terminals and the amount liberated when cholinergic neurons fire.