Abstract

The significance of the sympathetic nervous system in the secretion and metabolism of thyroid hormone in the mouse was studied by a combination of electron microscopic autoradiography, fluorescence histochemistry, light microscopy, and bioassay. In order to eliminate the influence of TSH, the secretion of this hormone was abolished by exogenous thyroxine. Sympathetic, norepinephrine (NE)-containing nerve terminals were present in a network around thyroid vessels and as single terminals close to thyroid follicles. Within 2 h after administration, 6-hydroxydopamine (6-OH-DA, 200 mg/kg iv) evoked a depletion of NE from thyroidal as well as from other sympathetic nerve terminals. Subsequently, 6-OH-DA caused a destruction of the terminals, demonstrable within 24 h. Administration of dopamine (DA) in the same dosage did not visibly affect the sympathetic nerve terminals. In animals, part of whose endogenous thyroid hormone had been labeled by 125I pretreatment, injection of 6-OH-DA or DA promoted the formation of numerous colloid droplets in thyroid follicle cells within 30 min, and increments of the blood 125I levels within 2 h. Although no further endocytosis occurred after the single injection of 6-OH-DA, there was a further blood 125I increment, with a maximum at about 24 h. Such a long-lasting increase was not seen after DA injection. If 6-OH-DA was given after the adrenergic nerve terminals had already been destroyed by previous 6-OH-DA treatment, the effects of 6-OH-DA and DA were similar; i.e., only short-lasting blood 125I increments (2 h maxima) were recorded. In animals pretreated with 125I-labeled T4, the elimination rate of the labeled hormone was reduced by a single injection of 6-OH-DA. The findings conform with previous studies indicating that the sympathetic nervous system can exert a direct, stimulatory effect on the secretion of thyroid hormone, by NE released from intrathyroidal adrenergic nerve terminals. In addition, the sympathetic nervous system seems to influence the peripheral metabolism of thyroid hormone.

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