Ahrén B
Department of Pharmacology, Lund University, Sweden.
Thyroidology. 1989 Dec;1(3):105-8.
The enzymes responsible for both the formation and degradation of gamma-aminobutyric acid (GABA) are known to exist in the thyroid gland. The thyroid is also equipped with high- and low-affinity uptake mechanisms for GABA. We therefore investigated the effects of GABA on basal and TSH-stimulated thyroid hormone secretion in the mouse according to the McKenzie technique. Iodine-deficient mice were pretreated with Na125I and thyroxine. GABA (1-100 nmol/kg iv) did not affect basal radioiodine levels. However, the neurotransmitter inhibited the TSH-induced increase in blood radioiodine levels. Thus, the increase after iv injection of TSH at 70 microU/animal (205 +/- 15%) was inhibited by GABA at 10 nmol/kg (to 155 +/- 14%; P less than 0.05). In contrast, a dose as high as 100 nmol/kg was necessary to inhibit the effect of TSH at its high dose of 350 microU/animal. The GABAA-receptor antagonist bicuculline counteracted this inhibitory action of GABA. Furthermore, pretreatment with the inhibitor of GABA-degrading enzyme GABA transaminase (gamma-vinyl GABA) impaired the stimulatory effect of TSH on blood radioiodine levels. Thus, at 350 microU/animal, TSH increased blood radioiodine levels by 363 +/- 34% in controls vs by only 246 +/- 32% in animals pretreated with gamma-vinyl-GABA (P less than 0.05). We conclude that GABA is an inhibitor of TSH-stimulated thyroid hormone secretion.
已知负责γ-氨基丁酸（GABA）合成和降解的酶存在于甲状腺中。甲状腺还具备对GABA的高亲和力和低亲和力摄取机制。因此，我们根据麦肯齐技术研究了GABA对小鼠基础状态下以及促甲状腺激素（TSH）刺激的甲状腺激素分泌的影响。对缺碘小鼠预先给予Na125I和甲状腺素。GABA（1 - 100 nmol/kg，静脉注射）不影响基础放射性碘水平。然而，这种神经递质抑制了TSH诱导的血液放射性碘水平升高。因此，以70微单位/只动物静脉注射TSH后放射性碘水平升高（205±15%），10 nmol/kg的GABA可将其抑制（降至155±14%；P<0.05）。相比之下，要抑制350微单位/只动物高剂量TSH的作用，需要高达100 nmol/kg的剂量。GABAA受体拮抗剂荷包牡丹碱可抵消GABA的这种抑制作用。此外，用GABA降解酶GABA转氨酶的抑制剂（γ-乙烯基GABA）预处理会削弱TSH对血液放射性碘水平的刺激作用。因此，在350微单位/只动物时，TSH使对照组血液放射性碘水平升高363±34%，而在预先用γ-乙烯基-GABA处理的动物中仅升高246±32%（P<0.05）。我们得出结论，GABA是TSH刺激的甲状腺激素分泌的抑制剂。
