Control of cyclic nucleotide metabolism by non-cholinergic, non-adrenergic nerves in rat thyroid gland.

Abstract

In addition to the well-established role of thyrotropin (TSH) in controlling metabolism and secretion of thyroid follicular cells1–3, there is evidence to suggest nervous (cholinergic and adrenergic) control mechanisms4–8. Nerves showing immunoreactivity to vasoactive intestinal peptide (VIP) have recently been demonstrated in the thyroid gland9, while exogenous VIP has been shown to elevate tissue cyclic AMP levels, increase the number of colloid droplets in follicular cells and increase thyroid hormone secretion in vivo. It was therefore suggested that VIP-containing nerves might control thyroid activity9, although a functional non-cholinergic, non-adrenergic innervation of the thyroid has not yet been demonstrated. By adopting the technique of electrical field stimulation previously used on isolated pancreatic segments10–13, we have studied cyclic nucleotide metabolism in isolated thyroid fragments and have now demonstrated directly the influence of both cholinergic and adrenergic as well as non-cholinergic, non-adrenergic nerves on thyroid cyclic AMP and cyclic GMP metabolism. In the presence of complete cholinergic and adrenergic blockade, nerve stimulation evoked complex time course changes in tissue cyclic AMP and cyclic GMP levels which could be mimicked precisely by VIP. Electrical stimulation of intrinsic thyroid nerves released, in addition to acetylcholine (ACh) and noradrenaline, a transmitter with the same action on thyroid cyclic nucleotide metabolism as VIP.