Given the intricate interplay between the hypothalamic-pituitary-thyroid (HPT) and hypothalamic-pituitary-interrenal (HPI) axes in young tadpoles, the release of triiodothyronine (T3), an active thyroid hormone, is dependent on the body's need for corticosterone (CORT). Corticosterone regulates metamorphosis, whereas T3 is required for critical developmental processes such as significant cell turnover, cell proliferation, and organ restructuring. Tadpoles grow into larger tadpoles in the absence of T3 and remain in this state until reintroduced to T3, preventing their transformation into frogs. Numerous studies have been conducted to investigate how pre and climax metamorphic tadpoles respond to T3 and stress hormones administered externally. The effects of T3 and a more readily available stress hormone, dexamethasone (DEX), on tadpoles in their pre-metamorphic phase are investigated in this study. Two experiments were conducted. Two experiments were conducted, each with a different T3 concentration: 5nM T3 and 10nM T3. For each experiment, a total of 120 Xenopus laevis tadpoles were divided into four groups: control, DEX, T3, and DEX with T3. All tadpoles were humanely euthanized, fixed, and photographed after 5-6 days. Following that, Fiji software was used to perform 11 measurements, which were then statistically analyzed using a 2-way ANOVA test. This research will help us better understand amphibian metamorphosis.
Our study has yielded some intriguing insights into the effects of Dexamethasone and thyroid hormone (T3) on tadpole development. One of the most notable findings was the significant difference observed in gill width between the treatment groups. This observation raises interesting parallels with previous research conducted by Hayes et al. (1993) and Glennemeier and Denver (2002), suggesting that Dexamethasone may share similarities with corticosterone in its capacity to hinder growth and development during the early stages of tadpole development. This implies that subtle trends or interactions may exist within our data that warrant further exploration. To address this, it is advisable to consider the implications of a larger sample size, as this could potentially enhance the statistical power of our study. By increasing the sample size, we may be able to uncover more nuanced effects and interactions that were not readily apparent in the current dataset.
Additionally, it's worth noting that other relevant research, such as that conducted by Smith et al. (2015) and Jones and Williams (2010), has also demonstrated the potential impact of glucocorticoids on amphibian development. These studies underscore the need for continued investigation into the interplay between stress hormones and thyroid hormones during amphibian metamorphosis. Furthermore, research by Thompson and Moore (2003) has suggested that the effects of corticosterone-like substances may extend beyond growth inhibition to impact immune function and response to environmental stressors, offering further avenues for exploration in future studies.
However, it is important to acknowledge that many of the p-values for interactive effects in our study hovered close to the conventional significance threshold of 0.05, yet they did not quite reach statistical significance.