Sympathetic nervous system activity in rat thyroid: potential role in goitrogenesis

Abstract

Young, James B., M. Elizabeth Bü rgi-Saville, Ulrich Bü rgi, and Lewis Landsberg. Sympathetic nervous system activity in rat thyroid: potential role in goitrogenesis. Am J Physiol Endocrinol Metab 288: E861-E867, 2005. First published December 7, 2004; doi:10.1152/ajpendo.00292.2004.-The role of sympathetic innervation in regulation of thyroid function is incompletely understood. We, therefore, carried out studies in rats utilizing techniques of norepinephrine turnover to assess thyroid sympathetic activity in vivo. Thyroidal sympathetic activity was increased 95% by exposure to cold (4°C), 42% by chronic ingestion of an iodine-deficient diet, and 32% in rats fed a goitrogenic diet (low-iodine diet supplemented with propylthiouracil). In addition, fasting for 2 days reduced sympathetic nervous system activity in thyroid by 38%. Thyroid growth and 125 I uptake were also compared in intact and decentralized hemithyroids obtained from animals subjected to unilateral superior cervical ganglion decentralization. Unilateral superior cervical ganglion decentralization led to a reduction in thyroid weight, in 125 I uptake by thyroid tissue, and in TSH-induced stimulation of 125 I uptake in decentralized hemithyroids. These results suggest that sympathetic activity in thyroid contributes to gland enlargement and may modulate tissue responsiveness to TSH. cold exposure; diet; fasting; iodine deficiency; pregnancy THE THYROID GLAND IS RICHLY innervated by autonomic nerves. Although the potential importance of this innervation was recognized well over 100 years ago (17, 25), the precise roles played by the adrenergic, cholinergic, and peptidergic components of the thyroid innervation in the regulation of glandular function are unclear even today. Because nerve endings have been noted in proximity to thyroid follicles (37, 39), a neural role in thyroid regulation appears likely. In vitro studies have provided considerable information regarding tissue and cellular responses to diverse biogenic amines and neuropeptides (1), although the contributions of these agents in vivo are largely unknown. This lack of information arises, in part, from the following problem. Because the potential effects of thyroid nerves are inhibitory as well as stimulatory, changes in thyroid function after either disruption or excitation of efferent neural pathways cannot be attributed to specific neural events. Furthermore, the principal methods employed to assess the activity of thyroid nerves in any given setting have been based on functional differences observed between intact and denervated thyroid glands. Consequently, assignment of specific effects to thyroid nerves is largely inferential.To circumvent this problem, we used a technique independent of glandular function to study thyroid neural physiology. Techniques of norepinephrine (NE) turnover assess the dynamic behavior of neuronal NE stores and provide a generally accepted index of the functional state of the sympathetic nervous system (SNS) in innervated tissues of unanesthetized, unrest...

Effects of acute and chronic relaxin-3 on food intake and energy expenditure in rats

“…The sympathetic nervous system (SNS) interacts closely with the HPT axis to regulate both energy expenditure and thyroid gland responsiveness to TSH. It is possible that suppression of TSH might be accompanied by modulation of the SNS both to normalize energy expenditure and normalize plasma T3 [25]. The effects of repeated H3 administration differ from those of other orexigenic peptides such as NPY, AgRP and ghrelin.…”

Expression of Opioid Growth Factor (OGF)–OGF Receptor (OGFr) Axis in Human Nonmedullary Thyroid Cancer

“…The OGF-OGFr axis increases p16 and p21 cyclin-dependent kinase inhibitors that decrease the phosphorylation of RB protein and block the transit of cells from G 1 to S phases of the cell cycle, thereby depressing cell proliferation (30,31). The source of OGF in thyroid tissues is unclear but may be autocrine, as well as paracrine from sympathetic nerve terminals, peri=parafollicular immunocytes, thyroid stroma interstitium, and=or endothelium of thyroidal vessels including capillaries (42,43). If the OGFOGFr system modulates cell replication and consequent growth in thyroid disorders through an inhibitory pathway, then administration of exogenous OGF, upregulation of endogenous OGF, attenuating the degradation of OGF, or increasing the number and=or affinity of OGF receptors could exert a potent negative influence on the progression of these malignant and nonmalignant conditions.…”

Neural innervation of white adipose tissue and the control of lipolysis

“…This method was used extensively by Landsberg and Young in their seminal studies of sympathetic drive under various metabolic challenges, diets and hormonal states ( e.g. , [172;312–314]). More specifically, the method is based on the uptake and subsequent decline in 3 NE such that fractional turnover (slope of the decline) and NETO [NE released per gram of tissue per hour [170]] can be determined.…”