Ahrén B, Hedner P
Department of Surgery, Lund University, Sweden.
Neuroendocrinology. 1989 May;49(5):471-5. doi: 10.1159/000125154.
The thyroid gland is richly innervated but the effects of activation of these nerves on thyroid hormone secretion are not yet established. In the present study, intravenous injection to mice of 2-deoxy-glucose (2-DG; 60 mumol/animal) was used to activate the autonomic nerves. The nerve activation occurs through the neuroglycopenia. We found that 2-DG inhibited the thyroid-stimulating hormone (TSH; 70 microU/animal)-induced thyroid hormone secretion, measured as release of radioiodine bound to anti-T4 in radioiodine-pretreated mice. This inhibition by 2-DG was completely reversed by the alpha-adrenoceptor antagonist phentolamine but not affected by the beta-adrenoceptor antagonist L-propranolol or the muscarinic receptor antagonist methyl-atropine. It is therefore concluded that neuroglycopenia-induced activation of the autonomic nerves inhibits TSH-induced thyroid hormone secretion by a mechanism that is reversed by phentolamine. It is suggested that it is mainly the adrenergic nerves that are involved in this action, and, consequently, that the function of the adrenergic nerves in thyroid physiology is to restrain the stimulatory action of TSH.
甲状腺有丰富的神经支配，但这些神经激活对甲状腺激素分泌的影响尚未明确。在本研究中，给小鼠静脉注射2-脱氧葡萄糖（2-DG；60 μmol/只动物）以激活自主神经。神经激活通过神经低血糖症发生。我们发现，在经放射性碘预处理的小鼠中，以与抗T4结合的放射性碘释放量来衡量，2-DG抑制促甲状腺激素（TSH；70 μU/只动物）诱导的甲状腺激素分泌。2-DG的这种抑制作用被α-肾上腺素能受体拮抗剂酚妥拉明完全逆转，但不受β-肾上腺素能受体拮抗剂L-普萘洛尔或毒蕈碱受体拮抗剂甲基阿托品的影响。因此得出结论，神经低血糖症诱导的自主神经激活通过一种可被酚妥拉明逆转的机制抑制TSH诱导的甲状腺激素分泌。提示主要是肾上腺素能神经参与此作用，因此，肾上腺素能神经在甲状腺生理学中的功能是抑制TSH的刺激作用。
