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Functional Connections between the Suprachiasmatic Nucleus and the Thyroid Gland as Revealed by Lesioning and Viral Tracing Techniques in the Rat

Netherlands Institute for Brain Research (A.K., A.N.F., J.W., R.M.B.), Meibergdreef 33, 1105 AZ Amsterdam, The Netherlands; Academic Medical Center (E.F.), Department of Endocrinology and Metabolism, F5–171, Meibergdreef 9, 1105 AZ Amsterdam

Address all correspondence and requests for reprints to: A. Kalsbeek, Netherlands Institute for Brain Research, Meibergdreef 33, 1105 AZ Amsterdam, The Netherlands. E-mail: A.Kalsbeek{at}nih.knaw.nl

Frequent blood sampling via intraatrial cannula revealed daily rhythms of TSH and thyroid hormones in both male and female Wistar rats. Thermic ablation of the biological clock, i.e. the suprachiasmatic nucleus (SCN), eliminated the diurnal peak in circulating TSH and thyroid hormones. In addition, SCN lesions produced a clear decrease of 24-h mean T₄ concentrations. A more pronounced effect of SCN-lesions on thyroid hormones, as opposed to TSH, suggested routes of SCN control additional to the neuroendocrine hypothalamo-pituitary-thyroid axis. Retrograde, transneuronal virus tracing was used to identify the type and localization of neurons in the central nervous system that control the autonomic innervation of the thyroid gland. In the spinal cord and brain stem, both the sympathetic and parasympathetic motorneurons were labeled. By varying the postinoculation survival time, it was possible to follow the viral infection as it proceeded. Subsequently, the pseudorabies virus (PRV) infected neurons in several brain stem cell groups, the paraventricular nucleus of the hypothalamus (PVN) and the central nucleus of the amygdala (second order labeling). Among PRV-infected neurons in the PVN were TRH-containing cells. Third order neurons were found in several hypothalamic cell groups, among which was the SCN. Therefore, we propose that the SCN has a dual control mechanism for thyroid activity by affecting neuroendocrine control of TSH release on the one hand and the autonomic input to the thyroid gland on the other.

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