Developmental and diel profiles of plasma corticosteroids in the bullfrog,Rana catesbeiana

Corticosteroids synergize with the thyroid hormone (TH) at late metamorphic stages and might have a role in the hormonal regulation of amphibian metamorphosis. This role could be influenced by diel fluctuations, particularly if the peak of the plasma corticoids changed in relation to the TH peaks. Diel variation in plasma corticosteroids was studied in Rana catesbeiana prometamorphic and climax tadpoles on 18:6, 12:12 and 6:18 light:dark (LD) cycles. Cortisol (hydrocortisone; HC) and aldosterone (ALDO) exhibited different, but LD cycle-specific, circadian fluctuations at prometamorphosis, whereas corticosterone (CORT) was undetectable (less than 1.18 ng/ml). HC, ALDO and CORT rhythms became synchronous at early metamorphic climax on all LD cycles, although the cosinor-derived acrophases, which occurred around the time of the dark:light transition, shifted approximately 6 h earlier from 18L:6D to 6L:18D. On both 18L:6D and 12L:12D, the acrophase of HC changed little from prometamorphosis to climax, whereas that of ALDO underwent a major phase shift. On 6L:18D, both the ALDO and the HC acrophases shifted at climax. These LD cycle-specific phase shifts of the diel rhythms placed the acrophases of the corticoids in different phase relationships to that of the previously determined thyroxine (T(4)) acrophase at climax, and may partially explain the influence of the light regimen on metamorphic timing. The pronounced diel variations in the corticoid concentrations from the troughs to the peaks show that hormone levels are a function of the time of day and the environmental lighting regimen, which need to be taken into account in measuring the level of plasma hormones in amphibians. The 24-h means calculated from the data of all the sampling times showed that only plasma ALDO and CORT, but not HC, rose markedly at climax, although there were significant LD cycle-related differences in the mean levels of both HC and ALDO at prometamorphosis, and in HC at climax. Additional work sampling at mid-light showed that plasma CORT peaked at Stage XXIII, decreased at the end of climax, and remained low in the postmetamorphic froglet at 2.1 ng/ml. In the adult bullfrog, CORT was clearly the predominant corticosteroid at 34.3 ng/ml, whereas HC and ALDO levels were only approximately 1.3 ng/ml.     

Cloning of a cDNA for Xenopus prolactin receptor and its metamorphic expression profile

A pituitary hormone, prolactin (PRL) shows various effects on cellular metabolism in amphibians, such as stimulation of larval tissue growth and inhibition of metamorphic changes. All these effects are mediated by its cell surface receptor. However, lack of information on PRL receptor (PRL-R) gene expression has made the physiological importance of the PRL/PRL-R system obscure in amphibian metamorphosis. Hence, a Xenopus PRL-R cDNA was cloned, its structure was characterized, and specific binding of PRL to Xenopus PRL-R expressed in COS-7 cells was confirmed. In adult tissues, high level expression was found in the lung, heart, brain, thymus and skin, and low level in the oviduct, kidney and spinal cord. The developmental expression pattern showed that PRL-R messenger ribonucleic acid (mRNA) was expressed in the brain and tail from premetamorphosis and the level increased toward late metamorphosis, suggesting that PRL may inhibit the metamorphic changes in those organs. The level of brain PRL-R mRNA reached a peak just at the start of the metamorphic climax stages and then decreased, whereas in the tail, mRNA expression peaked at late metamorphosis. In the kidney, mRNA expression increased and reached a maximum level at the end of metamorphosis. The results obtained were discussed in relation to metamorphosis.     

Adenohypophysial-thyroid activity of the tiger salamander, Ambystoma tigrinum, as a function of metamorphosis and captivity

The aim of this study was to determine the timing of adenohypophysial activation during metamorphosis of the tiger salamander, Ambystoma tigrinum. It consisted of two parts: 1) determination of plasma thyroid hormone concentrations and analysis of thyroid gland histology as a function of metamorphic stage and 2) analysis of the time-course of uptake of 125I by the thyroids during metamorphosis as an indicator of endogenous thyrotropin (TSH) levels. Significant increases in both triiodothyronine (T3) and thyroxine (T4) first were evident at the onset of metamorphic climax (stage II). Maximum levels of both hormones were not observed, however, until the completion of gill resorption (stage VII). No changes in thyroid histology were observed that could be unambiguously related to metamorphic transformation. The thyroids accumulated 125I in a slow but linear fashion in premetamorphic larvae (stage I). However, uptake exhibited a rapid peak during early climax (stage II), before maximum concentrations of thyroid hormones were observed. In addition, uptake was maintained above premetamorphic levels at stage VII, in conjunction with maximum levels of T4 and T3. Captivity alone produced a small but significant increase in plasma concentrations of T3. It produced no significant effect on either thyroid histology or uptake of 125I. These results indicate that adenohypophysial activation occurs rapidly and is maximal at the onset of metamorphic climax.     

Remodeling of insulin producing β-cells during Xenopus laevis metamorphosis

Insulin-producing β-cells are present as single cells or in small clusters distributed throughout the pancreas of the Xenopus laevis tadpole. During metamorphic climax when the exocrine pancreas dedifferentiates to progenitor cells, the β-cells undergo two changes. Insulin mRNA is down regulated at the beginning of metamorphic climax (NF62) and reexpressed again near the end of climax. Secondly, the β-cells aggregate to form islets. During climax the increase in insulin cluster size is not caused by cell proliferation or by acinar-to-β-cell transdifferentiation, but rather is due to the aggregation of pre-existing β-cells. The total number of β-cells does not change during the 8 days of climax. Thyroid hormone (TH) induction of premetamorphic tadpoles causes an increase in islet size while prolonged treatment of tadpoles with the goitrogen methimazole inhibits this increase. Expression of a dominant negative form of the thyroid hormone receptor (TRDN) driven by the elastase promoter not only protects the exocrine pancreas of a transgenic tadpole from TH-induced dedifferentiation but also prevents aggregation of β-cells at climax. These transgenic tadpoles do however undergo normal loss and resynthesis of insulin mRNA at the same stage as controls. In contrast transgenic tadpoles with the same TRDN transgene driven by an insulin promoter do not undergo down regulation of insulin mRNA, but do aggregate β-cells to form islets like controls. These results demonstrate that TH controls the remodeling of β-cells through cell-cell interaction with dedifferentiating acinar cells and a cell autonomous program that temporarily shuts off the insulin gene.     

Induction of lactogenic receptors. I. In the liver of hypophysectomized female rats.

To identify the hormones which affect lactogenic receptors in the liver of chronically hypophysectomized female rats, hormones were injected s.c. for 7 days. Specific binding (%, SB) of labelled ovine prolactin (PRL) in liver membrane preparations (1000,000 X g pellet) of controls was 1%. Estradiol (E2), cortisone (Con), ACTH or bovine growth hormone (bGH) treatment did not induce hepatic binding sites for PRL. Human GH and a single dose of 2mg PRL (but not lower doses) increased SB of PRL. Treatment with oPRL plus ACTH was less effective than hGH plus ACTH (13 vs 28%); combinations of oPRL plus Con as well as administration of oPRL plus ACTH to hypophysectomized and adrenalectomized female rats did not induce SB for PRL. Therapy with oPRL plus hGH (26%) was more potent than oPRL plus bGH (2%). These studies suggest that PRL, GH, and ACTH induce and in concert with sex steroids, modulate the lactogenic receptors in the female rat liver. The effect of ACTH is not due to increased adrenal corticoid secretion.     

The effects of corticosteroid hormones and thyroid hormones on lymphocyte viability and proliferation during development and metamorphosis of Xenopus laevis

Abstract. Metamorphosis in the South African clawed frog, Xenopus laevis , is characterized by a striking loss of lymphocytes in the thymus, liver, and spleen. Changes in the proliferative responses of splenocytes and thymocytes to T cell mitogens and semi-allogeneic cells are also observed at metamorphosis. Because the levels of circulating thyroid hormones (TH) and corticosteroid hormones (CH) increase dramatically during the climax of metamorphosis, we have investigated the possible role of TH and CH as mediators of the changes in lymphocyte numbers or lymphocyte function. Here we report on the in vitro effects of CH and TH on lymphocyte viability and on phytohemagglutinin-P (PHA)-stimulated lymphocyte proliferation at prometamorphosis and climax of metamorphosis. We have observed consistently significant inhibition of proliferation by corticosterone. In contrast, we have observed inconsistent inhibition of proliferation by both thyroxine (T₄) and triiodothyronine (T₃). In short-term studies, the viability of thymocytes and splenocytes was reduced in the presence of CH but not TH.
These observations are consistent with a hypothesis that loss of larval lymphocytes and changes of lymphocyte function at metamorphosis may be due to elevated concentrations of CH rather than TH.
Because CH have been shown to enhance TH-induced effects during metamorphosis, we looked at the combined effects of these agents on PHA-stimulated lymphocyte proliferation. While each agent was inhibitory in several experiments, there was no significantly greater inhibition when splenic lymphocytes were cultured with both.     

Heterochronic developmental shift caused by thyroid hormone in larval sand dollars and its implications for phenotypic plasticity and the evolution of nonfeeding development

Recent work on a diverse array of echinoderm species has demonstrated, as is true in amphibians, that thyroid hormone (TH) accelerates development to metamorphosis. Interestingly, the feeding larvae of several species of sea urchins seem to obtain TH through their diet of planktonic algae (exogenous source), whereas nonfeeding larvae of the sand dollar Peronella japonica produce TH themselves (endogenous source). Here we examine the effects of TH (thyroxine) and a TH synthesis inhibitor (thiourea) on the development of Dendraster excentricus, a sand dollar with a feeding larva. We report reduced larval skeleton lengths and more rapid development of the juvenile rudiment in the exogenous TH treatments when compared to controls. Also, larvae treated with exogenous TH reached metamorphic competence faster at a significantly reduced juvenile size, representing the greatest reduction in juvenile size ever reported for an echinoid species with feeding larvae. These effects of TH on D. excentricus larval development are strikingly similar to the phenotypically plastic response of D. excentricus larvae reared under high food conditions. We hypothesize that exogenous (algae-derived) TH is the plasticity cue in echinoid larvae, and that the larvae use ingested TH levels as an indicator for larval nutrition, ultimately signaling the attainment of metamorphic competence. Furthermore, our experiments with the TH synthesis inhibitor thiourea indicate that D. excentricus larvae can produce some TH endogenously. Endogenous TH production might, therefore, be a shared feature among sand dollars, facilitating the evolution of nonfeeding larval development in that group. Mounting evidence on the effects of thyroid hormones in echinoderm development suggests life-history models need to incorporate metamorphic hormone effects and the evolution of metamorphic hormone production.     

Variation in thyroid hormone action and tissue content underlies species differences in the timing of metamorphosis in desert frogs

Hormonal control of post-embryonic morphogenesis is well established, but it is not clear how differences in developmental endocrinology between species may underlie animal diversity. We studied this issue by comparing metamorphic thyroid hormone (TH) physiology and gonad development across spadefoot toad species divergent in metamorphic rate. Tissue TH content, in vitro tail tip sensitivity to TH, and rates of TH-induced tail tip shrinkage correlated with species differences in larval period duration. Gonad differentiation occurred before metamorphosis in species with long larval periods and after metamorphosis in the species with short larval periods. These differences in TH physiology and gonad development, informed by phylogeny and ecology of spadefoot metamorphosis, provide evidence that selection for the short larval periods in spadefoot toads acted via TH physiology and led to dramatic heterochronic shifts in metamorphic climax relative to gonad development.     

Does adrenal cortex influence prolactin secretion? Evaluation in hirsute women

To define the role of adrenal hormones on PRL secretion, we investigated 28 women by administering i.v. 0.25 mg. ACTH (h 8.00) every 45' for 135' to better evaluate any relationship between enhanced adrenal steroidogenic activity (both glycoactive and androgenic) and PRL secretion. Blood samples were drawn at 0', 45', 90', 135', and PRL, F, DHEAS, and 170HP were measured by RIA methods. A significant lowering of PRL levels and a concomitant enhancement of steroid plasma levels were found. Our data are in line with those found by some Authors who observed the lack of PRL enhancement after hypoglycemia during glucocorticoid administration and the absence of nocturnal peak of PRL in patients with Cushing's disease. However statistical evaluation (linear analysis regression) of data obtained provides further evidence for the extremely influential role played by adrenal gland hormones on PRL secretion in women.     

Plasma LH, FSH, testosterone, prolactin and androstenedione in male white-tailed deer after ACTH and dexamethasone administration

1. In order to investigate the role of the adrenocortical system in the regulation of plasma levels of reproductive hormones, adult male white-tailed deer (five intact and one castrated) from a captive herd were sedated with xylazine and ketamine and then challenged with various doses of ACTH with and without dexamethasone (DX) pretreatment. 2. Plasma levels of LH, testosterone (T), FSH, prolactin (PRL) and androstenedione (A) were determined by RIA in serial samples taken from the jugular vein. 3. An increase of A levels detected after ACTH in both intact and castrated deer indicated stimulation of secretion of adrenal androgens by ACTH. 4. No effect on FSH and PRL levels was observed in either group. 5. A significant decline of LH and T observed in various treatments could not be attributed to ACTH or DX administration. It is speculated that the decrease may be caused by anaesthetics which alleviate the stress induced in deer by the pre-immobilization activities.     

Metamorphosis of summer flounder, Paralichthys dentatus: cell proliferation and differentiation of the gastric mucosa and developmental effects of altered thyroidal status.

Summer flounder, like most marine fishes studied to date, are stomachless at first feeding, and subsequently acquire gastric function during the process of metamorphosis. Stomach formation is controlled largely by thyroxine (T4). In the present work we sought to understand gastric organogenesis in terms of cell proliferation and its relationship to histological differentiation. The objectives of the study were (1) to obtain a developmental pattern of cell proliferation in the gastric mucosa and to relate that pattern to the progress of gastric differentiation; and (2) to understand the regulatory role of T4 on cell proliferation and histological differentiation by altering the thyroidal status of the developing larvae. We observed that (1) in normally developing larvae, cell proliferation increased by early metamorphic climax (MC), remained high until mid-MC, and decreased to basal levels by late MC; concomitantly, the gastric glands appeared and differentiated in the fundic mucosa, and were complete by late MC; (2) T4 accelerated the differentiation of gastric glands and mucus neck cells, while inhibiting the concomitant increase in cell proliferation observed in controls; and (3) the goitrogen thiourea inhibited both cell proliferation and gastric differentiation compared to controls. These results indicate that T(4) is necessary for the three-fold increase in cell proliferation that occurs in early metamorphic climax, but that high T4 levels promote differentiation at the expense of proliferation. The observed effects would be consistent with the normal, metamorphosis-related increase in whole body T4.     

Tissue-specific regulation of type III iodothyronine 5-deiodinase gene expression mediates the effects of prolactin and growth hormone in Xenopus metamorphosis

Prolactin (PRL) and growth hormone (GH) are known to be able to act as antimetamorphic hormones. From investigations of how PRL inhibits Xenopus tail regression in vitro, it was found that the both hormones could, in addition to their known antimetamorphic actions, upregulate mRNA expression of type III iodothyronine 5-deiodinase (5D), an enzyme that inactivates thyroid hormones (TH). Conversely, both PRL and GH were found to downregulate 5D mRNA expression in the liver. Blockage by PRL of TH-induced tail regression in organ culture was released by treatment with iopanoic acid (IOP, an inhibitor of 5D activity). The IOP-released tail regression displayed a unique morphology of the larger fins retained on the regressing tails, consistent with the finding that mRNA for both PRL receptor and 5D were enriched in the fin. The results suggest that the metamorphosis-modulating actions of PRL and GH are mediated, at least partially, by tissue-specific regulation of 5D mRNA expression.     

Effects of acute alcohol intoxication on pituitary-gonadal axis hormones, pituitary-adrenal axis hormones, beta-endorphin and prolactin in human adolescents of both sexes

Teenage drinking continues to be a major problem in industrialized countries, where almost 35% of alcohol drinkers are under 16 years old. In the present paper we studied the effects of acute alcohol intoxication (AAI) on the pituitary-gonadal (PG) axis hormones, and the possible contribution of pituitary-adrenal (PA) axis hormones, beta-endorphin (BEND), and prolactin (PRL) to the alcohol-induced dysfunction of PG axis hormones. Blood samples were drawn from adolescents that arrived at the emergency department with evident behavioral symptoms of drunkenness (AAI) or with nil consumption of alcohol (controls [C]). Our results demonstrated that AAI produces in adolescents a high increase in plasma PRL, ACTH, and cortisol (F), and a contradictory behavior of testosterone (T) according to gender: plasma T was increased in females and decreased in males. ACTH and PRL correlated positively with F, dehydroepiandrosterone-sulphate (DHEAS) and T in females, which suggests that PRL and ACTH could synergistically stimulate adrenal androgen production. In contrast, the decrease in T and increase in BEND in males suggests that AAI could have an inhibitory effect on testicular T, perhaps mediated by BEND. The hormones studied are involved in the development of secondary sexual characteristics and the growth axis during adolescence. The deleterious effects of alcohol abuse should be made known to adolescents and the appropriate authorities.     

Identification of source of excessive ACTH production by improved selective venous sampling: simultaneous assay of PRL as a pituitary marker

To identify an obscure site of excessive ACTH production, selective venous sampling was performed by Seldinger's method in a 32-year-old man. Differential diagnosis between an ectopic ACTH producing tumor and Nelson's syndrome was quite inconclusive in this patient in spite of extensive clinical and laboratory evaluations, including pituitary surgery. In this study, PRL was measured in every sample as a reliable marker for pituitary drainage. Significantly higher rations (2.6 to 5.3) of catheter to peripheral (C/P) concentration of PRL at sites closer to the pituitary indicated successful samplings of pituitary drainage. C/P ratios of ACTH correlated very closely (correlation coefficient = 0.906, p less than 0.01) with those of PRL at every sampling site. Thus, it was concluded that the site of excessive ACTH production in this patient was in the pituitary gland. The methods applied in this study appear to be useful in differentiating ectopic from eutopic production of other pituitary hormones as well.     

The decrease in plasma melatonin at metamorphic climax in Rana catesbeiana (bullfrog) tadpoles is induced by thyroxine.

Melatonin decreases in the plasma of Rana catesbeiana (bullfrog) tadpoles at the climax of metamorphosis when the thyroxine (T(4)) level peaks. Since melatonin inhibited thyroid function in vitro, it would be of interest to determine if the decline in plasma melatonin permits greater thyroid hormone secretion, or if the increasing levels of T(4) cause the climactic decrease in plasma melatonin. The reciprocal effects of administering T(4) or melatonin just prior to metamorphic climax were examined in tadpoles kept at 22 degrees C on an 18L:6D cycle. If melatonin functions as a thyroid antagonist at later metamorphic stages, administration of melatonin should decrease plasma T(4), whereas if T(4) causes the decline in plasma melatonin, T(4) treatment of tadpoles prior to climax should induce the climactic melatonin decrease prematurely. Once daily injection of 40 microg melatonin for 5 days at 19.30 h had no effect on metamorphic progress, or on plasma T(4) or melatonin levels, except for a transient rise in melatonin just after the injection. Immersion in 2.2x10(-4) M melatonin for 6 days accelerated metamorphosis and decreased plasma melatonin, but had no effect on plasma T(4). Administration of T(4) by injection of 0.2 microg, or immersion in a 6.3x10(-8) M solution accelerated metamorphosis more than melatonin immersion, raised plasma T(4) to climax levels, and induced a decrease in plasma melatonin. We conclude that rapid clearance of exogenous melatonin from the circulation in these experiments did not allow it to affect plasma T(4), and that there is clear evidence that the rise in T(4) induces the climax decrease in plasma melatonin. The finding that immersion in a high level of melatonin can lower plasma melatonin and accelerate metamorphosis, whereas a single daily injection does not, provides an explanation for some of the contradictory reports in the literature concerning melatonin's effect on tadpole metamorphic progress.     

Direct influence of melatonin on the thyroid and comparison with prolactin

Melatonin administered in vivo had previously been shown to inhibit thyroid cell proliferation and subsequent in vitro thyroxine (T(4)) secretion in anuran tadpoles. Melatonin in vitro also directly reduced the sensitivity of the thyroid to thyrotropin (TSH). The present work sought to determine whether melatonin directly affected baseline, unstimulated T(4) secretion, and to compare its effect with that of prolactin (PRL). Thyroids from larval Rana catesbeiana or adult Rana pipiens were incubated in control or melatonin (0.01 to 100 microg/ml) media. Melatonin directly inhibited T(4) secretion by thyroids from both tadpoles and frogs at all concentrations of melatonin used and at both prometamorphic and climax tadpole stages. PRL, used in vitro at 10 microg/ml, did not influence the response of the thyroid to TSH (0.2 microg/ml) in young tadpoles, or the baseline secretion of T(4) by thyroids at any stage of larval life except climax, when T(4) secretion was significantly decreased by the third day of culture. Thus although both melatonin and PRL have been shown to antagonize the action of T(4) in vitro, and to decrease metamorphic rate, melatonin is a much more effective thyroid gland inhibitor than PRL.     

The meal-related peak in plasma cortisol is not mediated by radioimmunoassayable ACTH

There is evidence for the existence of ACTH-unrelated mechanisms in the regulation of cortisol secretion in man. The present study was designed to elucidate the interrelations between plasma ACTH and cortisol levels during the 'midday surge' in cortisol concentrations. For comparison, a 'midday surge' was imitated by infusing small amounts of ACTH in dexamethasone-suppressed subjects. The meal-related cortisol bursts were not preceded by an adequate increase in ACTH levels. In contrast, markedly elevated ACTH levels were necessary to produce a comparable cortisol peak by administration of ACTH. Apparently, the meal-related bursts in cortisol levels were not mediated by radioimmunoassayable ACTH. These findings argue against the classic concept that the adrenal cortex is inseparably linked to immediately preceding hormonal events occurring in the hypothalamo-pituitary system.     

Early larval development and metamorphosis in the summer flounder: changes in per cent whole-body water content and effects of altered thyroid status

At the end of premetamorphosis, summer flounder Paralichthys dentatus larvae had 84·1% whole-body water content (WBW), which decreased to the lowest levels (8·5%) at the start of metamorphic climax (MC). During mid- and late MC, %WBW was slightly higher (82·1%) then returned to the lowest levels at the juvenile stage. In fish treated with thyroxine (T₄-Na salt, 100 ng ml⁻¹) beginning at premetamophosis, %WBW never differed from controls of the same age throughout metamorphosis, despite an earlier start of metamorphic climax and transitional settling behaviour. This suggests that thyroid hormones do not mediate the drop in %WBW which accompanies natural metamorphosis. Thiourea (TU, 30 μg ml⁻¹) treatment of fish over the same period induced a developmental stasis in early MC which was accompanied by initially higher %WBW than controls at 33 days post-hatch, followed by a progressive decrease to abnormally low %WBW by 42 and 45 days post-hatch. Since concurrent treatment with TU+T₄ rescued the fish from both the TU-induced developmental stasis and abnormally low %WBW, these findings suggest that thyroid hormones, or thyroid hormone-mediated developmental progression, are necessary for regulating %WBW.     

In vitro secretion of ACTH, beta-endorphin and beta-lipotropin in Cushing's disease and Nelson's syndrome

Tissue from histologically confirmed ACTH cell adenomas in Cushing's disease (CD) and Nelson's syndrome (NS) was gained by transsphenoidal surgery. Combined enzymatic and mechanic agitation of tumor tissue yielded a cell suspension. Aliquots of the cell suspension were transferred to superfusion chambers immediately after isolation and investigated for ACTH and beta-endorphin production. Feedback action of cortisol (CO) and dexamethasone on basal hormone production and on lysine vasopressin (LVP) induced ACTH secretion were studied. Adenomatous tissue and anterior lobe tissue from the same patient in CD could be investigated simultaneously in 4 cases. The paraadenomatous tissue showed depression of basal and LVP-induced ACTH secretion. In all adenomatous tissues investigated there was missing or reduced suppression of basal ACTH secretion by physiological levels of CO. CO not only failed to suppress LVP-induced ACTH secretion but also seemed to enhance LVP stimulation in some experiments. This study confirms former results, that a missing or inversed feedback action or glucocorticoids in adenoma cells is a mechanism involved in the pathological ACTH secretion in CD and NS. Bioassayable and immunoreactive ACTH from media of superfusion and short-term static incubation were compared with beta-endorphin and beta-LPH in an assay detecting these two peptides with equimolar sensitivity. Secretory patterns were basically parallel but great differences showed in quantities of hormones secreted. In addition, Sephadex G-50 gel chromatography was performed to separate beta-endorphin from beta-LPH and to calculate the ratios. These profiles show great variations between different adenomas.     

黑斑蛙变态过程中甲状腺发育及甲状腺激素分泌

系统研究了我国本土两栖动物种黑斑蛙（Rana nigromaculata）变态发育过程中甲状腺组织学和甲状腺激素水平的变化,为甲状腺生物学和甲状腺干扰研究提供基础数据。黑斑蛙蝌蚪发育的形态变化: 第26-40阶段,后腿芽生长并逐渐分化出五趾结构;42阶段,开始进入变态高峰期,前肢展开,尾吸收,蝌蚪身体发生巨大形变;46阶段,蝌蚪完全变态成小蛙。随着形态学的变化,甲状腺的组织结构也发生明显的变化: 26-37阶段,甲状腺体积较小,增长缓慢;38阶段甲状腺体积迅速膨大,进入高峰期,甲状腺的发育达到顶峰;随着变态完成,甲状腺又逐渐缩小。甲状腺组织学变化的同时,甲状腺激素水平也相应发生变化: 在变态前期,下颌中3,3',5-三碘代-L-甲腺原氨酸（T3）水平增长缓慢,进入变态期后,T3含量迅速升高,在变态高峰期达到峰值,随后下降。以上结果表明,黑斑蛙发育过程中甲状腺组织学的变化与甲状腺激素水平的波动相吻合。对黑斑蛙甲状腺系统的研究,可为日后使用黑斑蛙开展甲状腺干扰作用的研究提供基础。