Thyroid hormones act at the level of the pituitary to regulate thyrotropin and growth hormone secretion in hatchling slider turtles (Pseudemys scripta elegans)

Abstract

Pituitaries from hatchling turtles (Pseudemys scripta elegans) were incubated with different doses of L-thyroxine (T4: 1-500 ng/ml) or 3,5,3'-triiodothyronine (T3: 1-50 ngiml) for various times (1-48 hr) to assess their effects on basal thyrotropin (TSH) and growth hormone (GH) secretion and responsiveness to thyrotropin-releasing hormone (TRH: 10 ngiml). Pretreatment with a pharmacological dose of T4 (500 ngiml) for 1 hr inhibited the TSH response to TRH, and physiological doses were effective after slightly longer times. The TRH effect was reduced by exposure to 50 ngiml T, for 1 hr, and abolished after 4 hr. Pretreatment with 50 ngiml T, or T, for 6 hr did not affect basal TSH secretion, but the attenuation of the TRH response persisted for at least 20 hr after removal of thyroid hormones. Longer exposure (16 hr) to 50 ngiml T4 or T3 reduced both TSH basal secretion and the response to TRH. A low dose (1 ngiml) of T4 or T, for the same amount of time had no effect on basal TSH secretion and only slightly reduced the TRH response; T3 was more potent than T4. Basal secretion and TRH responses of glands pretreated with 5 ng/ml T4 were not different from controls after 4 and 6 hr, but were significantly reduced after 24 hr of exposure; 15 ng/ml T4 reduced the TRH response after 6 hr, but basal secretion was not affected until 24 hr. Treatment with 2 ng/ml T, for 48 hr reduced the response to TRH but did not affect the baseline. Basal and TRH-stimulated GH secretion was also inhibited by thyroid hormones, but the onset of these effects were delayed (16 to 24 hr after exposure) and required a relatively high dose (50 ng/ml).These data are consistent with an earlier report from this laboratory (Denver and Licht: J . Exp. Zool. [in press], '88) that in vivo treatment with thyroid hormone or a goitrogen alters in vitro pituitary hormone secretion in turtles and provide evidence for a direct action of thyroid hormones at the level of the pituitary.The mammalian hypothalamo-hypophyseal-thyroid axis has long been considered a classic example of a negative-feedback loop, with thyroid hormones (TH) determining the set-point for pituitary thyrotropin (TSH) secretion. It has been established that the primary site of TH feedback regulation of pituitary TSH secretion in mammals is at the level of the thyrotrope (see Morley , '8l>, although compelling evidence for an important role of TH in the regulation of hypothalamic TRH secretion was recently presented (Segerson et al., '87). The nature of the thyroidal feedback in nonmammalian vertebrates is poorly understood. In particular, the paucity of data describing changes in the functional status of the pituitary or the hypothalamus in relation to thyroidal state prohibits evaluation of hypotheses regarding the site(s) of action of TH in relation to the secretion of TSH or any other hormones.Previous work from this laboratory demonstrated that turtle pituitaries respond in vitro to the tripeptide amide, thyrotropin-releasing hormone (TRH) by releasing TSH, prolactin (PRL), ...

Evidence for a negative feedback in the control of eel growth hormone by thyroid hormones

“…A similar conclusion was previously raised in view of the similar efficiency of both T 3 and T 4 to inhibit TSH mRNA levels in eel pituitary cells, in the same culture conditions (Pradet-Balade et al 1997). In the turtle, T 3 and T 4 also had similar inhibitory effects on GH secretion in vitro (Denver & Licht 1988). In contrast, in the domestic fowl, T 3 , but not T 4 , has been shown to inhibit GH secretion in vitro (Harvey et al 1991).…”

“…In vivo, hypothyroidism is a potent stimulator of GH secretion, and exogenous THs markedly suppress GH release (Harvey 1990b, Harvey et al 1991. A negative effect of T 3 on GH synthesis and release has also been documented in vitro in birds (Denver & Harvey 1991) and similarly, T 3 is reported to exert inhibitory effects on GH release in vitro in chelonid reptiles (turtles: Denver & Licht 1988). These data from cattle, humans, birds and reptiles suggest that the more generalized vertebrate pattern of thyroidal regulation of pituitary GH may be inhibitory (Denver & Harvey 1991).…”

“…T 3 also suppressed basal as well as TRH-or growth hormone-releasing hormone (GHRH)-induced GH secretion in vivo in euthyroid and hypothyroid chicken (Scanes & Harvey 1989), an inhibitory effect also evidenced in vitro (Harvey 1990b). In chelonian reptiles, THs were shown to act directly at the level of the pituitary to inhibit basal and TRH-induced GH secretion in vitro (Denver & Licht 1988). In humans, although THs are required for normal GH secretion (Valcavi et al 1992, Müller et al 1999, they have also been shown to reduce it in vivo in hyperthyroid patients (Sazaki et al 1985) and in adolescents with thyrotoxicosis (Finkelstein et al 1974).…”

Basic transcription element binding protein is a thyroid hormone‐regulated transcription factor expressed during metamorphosis in Xenopus laevis

“…Thyroxine radioimmunoassay Plasma T 4 concentration was determined by radioimmunoassay (RIA; Mackenzie & Licht 1984; Denver & Licht 1988). Primary antiserum for T 4 was purchased from Dr Viggo Kruse (Denmark).…”

Growth in Reptiles

“…Little is known about the endocrinology of growth in reptiles [47][48][49], At an ecological level, a great deal more work needs to be carried out to determine the significance of low growth rates -why do some species grow slowly? More work is also needed on the genetics of reptilian growth and the adaptive significance of intraspecific dif ferences in growth rates.…”