Neurotransmitter Regulation of Thyroid Activity

Maayan, Morelly L.; Volpert, Eugene M.; Debons, Albert F.

doi:10.3109/07435808709023673

Cited by 10 publications

(3 citation statements)

References 58 publications

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“…On the other hand, an inhibitory effect of an increase in intracellular Ca2+ on thyroid gland is also widely recognized (20). Unger et al demon¬ strated that carbamylcholine inhibited the TSHstimulated prelabelled butanol-extractable release of 'i from dog thyroid slices by blocking the for¬ mation of pseudopods (21).…”

Section: Discussionmentioning

confidence: 98%

Inhibitory effects of ionophore A23187 on the release of thyroid hormone and colloid reabsorption in mouse thyroid glands

Mori-Tanaka

Tajima²,

Miyagawa³

et al. 1991

Acta Endocrinologica

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The effect of the ionophore A23187 on a. the release of thyroid hormone from perifused mouse thyroid glands and b. the morphological changes in follicular epithelial cells was evaluated. A23187 at a concentration of 5 \g=m\mol/lsignificantly inhibited both the TSH-and the forskolin-stimulated release of T3 and T4. In the presence of 3-isobutyl-1-methylxanthine or (4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone) RO 20-1724, A23187 did not affect the forskolin-stimulated release of cAMP, but did inhibit the release of T3 and T4 stimulated by forskolin. Light and electron microscopic evaluation of the follicular epithelial cells of mouse thyroid tissues following 1-h stimulation with forskolin showed numerous pseudopods engulfing luminal colloid of various size and the presence of reabsorbed colloid droplets in the apical cytoplasm. Quantitative electron microscopic analysis revealed that the addition of the ionophore A23187 reduced the number of reabsorbed colloid droplets to one eighth in follicular epithelial cells. These observations suggest that the increase in intracellular Ca2+ induced by the ionophore A23187 inhibits the TSH-stimulated thyroid hormone release independently of the cAMP level, and that the suppression of thyroid hormone release may be due to an inhibition of colloid reabsorption. Intracellular Ca + plays an important role in the regulation of cell function in many biological sys¬ tems, especially in respect to exocytosis and secre¬ tion (1). However, an inhibitory effect of an in¬ crease in intracellular Ca2+ in the thyroid has been reported (2-4). The ionophore A23187 and carbamylcholine, both of which increase the influx of calcium, inhibit the TSH-stimulated production of cAMP (2-4) and the secretion of iodine (4). We re¬ cently showed that, in rat thyroid glands, A23187 inhibited both the TSH-induced morphological changes in the follicular epithelial cells and the TSH-stimulated release of T3 without reducing the cAMP level (5).The present experiment was designed to inves¬ tigate further the mechanism by which an increase in intracellular Ca2+ attenuates the release of thy¬ roid hormone using a mouse thyroid perifusion system, which has been found useful in studying thyroid function in vitro (6). In this experiment, we quantitatively evaluated the ultrastructural changes induced by forskolin in the follicular epi¬ thelial cells with dynamic observation of the release of thyroid hormone by the agent. Materials and MethodsPerifusion of the mouse thyroid gland was performed as previously described (5-8). Thyroid glands were obtained from BALB/c or ddY mice (8-10 weeks) under ether an¬ esthesia. The excised glands were pre-incubated in KrebsRinger bicarbonate buffer, pH 7.4, containing 0.1% glu¬ cose and 0.3% BSA (KRBG) at 37°C for 90 min. Twenty pre-incubated thyroid halflobes were placed in a chamber and perifused with the same buffer at a flow rate of 1.9 ml/20 min. KRBG was used as the infusion buffer for an initial period of 60 min. After washing with Ca2+-free KRBG for 10 min, the buffer...

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Section: Discussionmentioning

confidence: 98%

Inhibitory effects of ionophore A23187 on the release of thyroid hormone and colloid reabsorption in mouse thyroid glands

Mori-Tanaka

Tajima²,

Miyagawa³

et al. 1991

Acta Endocrinologica

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“…In accordance with earlier investigations (Melander & Rerup 1968;Ahren et al 1986) the present results from TCA precipitation and butanol extraction indicate that a considerable part of the total lZ5I in blood from animals prepared according to the McKenzie technique (1958) may be non-hormonal. The desirability of more hormone-specific methods is thus obvious, and has recently been emphasized (Maayan et al 1987).…”

Section: Discussionmentioning

confidence: 99%

Determination of Thyroxine Release in Vivo: A Simple, Specific and Sensitive Method in Mice

Hedner

Bengtsson

Åhrén

1988

Pharmacology & Toxicology

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When thyroid hormone secretion in vivo was studied by the release of 125I from thyroid to blood after TSH in mice preloaded with the isotope, only 54.4 +/- 2.0% (+/- SE) of plasma 125I was butanol extractable, indicating low specificity for thyroid hormones. To improve specificity plasma 125I was bound to anti-T4 rabbit antibodies and precipitated with goat antirabbit serum. The intraassay coefficient of variation was 2.5%, and anti-T4 bound radioactivity correlated well with that extractable with butanol (r = 0.95, P less than 0.001). The effect of 40-1000 microU TSH intravenously in mice pretreated with 1 microgram T3 3 times during 2 days to suppress endogenous TSH was evaluated 2 hrs after the injection of TSH by 1) conventional radioimmunoassays of total and free stable T4 in plasma (no preloading with 125I), 2) total blood 125I in mice preloaded with 125I, and 3) anti-T4 bound 125I in plasma in mice preloaded with 125I. Stable T4 increased with TSH doses of 70 microU or higher, but the slope was low and the relation between error variance and slope did not permit a useful bioassay. Total blood 125I responded significantly to 40 microU TSH and showed a favourable relation between error variance and slope, but the specificity may be questioned. Anti-T4 bound 125I in plasma also responded significantly to 40 microU TSH and showed a very good relation between error variance and slope. The new technique of measuring anti-T4 bound radioactivity seems to combine the specificity of radioimmunoassay with a precision and sensitivity well comparable to that of the conventional radioiodine release technique.

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“…Также установлено, что полное удаление из инкубационной среды ионов Ca 2+ не изменяло действия норэпинефрина. Что касается ингибирующего влияния L-допамина на секрецию тиреоидных гормонов, то эф-фект, по-видимому, опосредуется активацией дофамино-вых рецепторов тироцитов [11].…”

Section: симпатическая системаunclassified

Nervous Regulation оf Thyroid Function

Lychkova¹

2013

ARAMS

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Nervous Regulation оf Thyroid Function Review examines the autonomic regulation of thyroid function. Review examines the issues of autonomic regulation of the thyroid gland. Activation of the central α-adrenergic mechanisms increases the release of thyroid-stimulating hormone of pituitary mainly due to the stimulation of its secretion. Dopamine inhibits the secretion of this hormone ВведениеЩитовидная железа (ЩЖ) -эндокринная железа позвоночных, депонирующая йод и вырабатывающая йодосодержащие гормоны (йодтиронины), участвующие в регуляции обмена веществ и росте отдельных клеток и организма в целом. Синтез тироксина (тетрайодтиро-нина, T 4 ) и трийодтиронина (T 3 ) происходит в эпители-альных фолликулярных клетках (тироцитах). Кальци-тонин, пептидный гормон, синтезируется парафолли-кулярными С-клетками и регулирует уровень кальция в сыворотке. Транскрипты гена кальцитонина кодируют также пептид, известный как кокальцигенин (кальцито-нин ген-ассоциированный пептид, CGRP).Функция ЩЖ регулируется гипоталамо-гипофизар-но-тиреоидной системой, в т.ч. тиреотропин-рилизинг гормоном (ТРГ), синтезируемым гипоталамусом, тире-отропным гормоном гипофиза (ТТГ). ТРГ стимулирует синтез и секрецию ТТГ независимо от наличия или от-сутствия тиреоидных гормонов. Деструкция участка ги-поталамуса, синтезирующего ТРГ, приводит к развитию гипотиреоза. В свою очередь, синтез ТРГ регулируется уровнем гормонов ЩЖ в крови, омывающей гипотала-мус, по принципу отрицательной обратной связи. ЩЖ в основном секретирует Т 4 . Практически весь пул (80%) циркулирующего в крови Т 3 образуется за счет процессов тканевого дейодирования Т 4 в печени и почках. Именно избыточное содержание Т 3 подавляет синтез и секрецию ТТГ. Двойственное влияние ТРГ и тиреоидных гормонов является основным механизмом управления концентра-цией ТТГ в крови. ТТГ, в свою очередь, регулирует синтез тиреоидных гормонов, пролиферацию тироцитов, кро-воснабжение железы, что в совокупности обеспечивает поддержание концентрации гормонов ЩЖ на необходи-мом для индивида уровне [1].Особое место в регуляции функции ЩЖ занимают нейротрансмиттеры, среди которых ведущее значение придают катехоламинам, серотонину, ацетилхолину, ги-стамину и оксиду азота. Механизмы нейромедиаторной регуляции тиреоидной функции изучены недостаточно.

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Neurotransmitter Regulation of Thyroid Activity

Cited by 10 publications

References 58 publications

Inhibitory effects of ionophore A23187 on the release of thyroid hormone and colloid reabsorption in mouse thyroid glands

Inhibitory effects of ionophore A23187 on the release of thyroid hormone and colloid reabsorption in mouse thyroid glands

Determination of Thyroxine Release in Vivo: A Simple, Specific and Sensitive Method in Mice

Nervous Regulation оf Thyroid Function

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