Temperature dependence of in vitro pituitary, testis, and thyroid secretion in a turtle, Pseudemys scripta

In vitro culture was used to examine the direct actions of temperature at the level of pituitary hormone [luteinizing hormone (LH), thyrotropin (TSH), growth hormone (GH), prolactin (PRL)] responses to neuropeptides and two related peripheral endocrine responses [thyroid hormone (T4) and testicular androgen secretion] to pituitary hormones (TSH and gonadotropins) in a turtle, Pseudemys scripta. All these responses were fully suppressed at very low temperatures (5-6 degrees) and maximal near the species' preferred body temperature (28 degrees), but sensitivities differed markedly in intermediate ranges. At the pituitary level, the response of TSH, GH, and PRL to thyrotropin-releasing hormone (TRH) was considerably more temperature sensitive than the response of LH to gonadotropin-releasing hormone (GnRH) stimulation. TSH, GH, and PRL were unresponsive at 20 degrees or below, whereas LH secretion was stimulated almost equally between 12 and 28 degrees; the main effect of cooling on LH secretion was to reduce the duration of the response to GnRH. There was no clear effect of previous thermal history on temperature sensitivity of pituitary neuropeptide responsiveness although the general responsiveness of the gland was altered; however, these latter effects may also be related to variations in other factors such as photoperiod, season, and nutrition. Temperature sensitivities of the thyroid and testes also differed, but in the opposite way from the related pituitary cell types. Thyroid glands were relatively insensitive to temperature and responded to TSH between 12 and 32 degrees, with no difference between 20 and 28 degrees. In contrast, testicular androgen secretion showed an abrupt decline in gonadotropin responsiveness below 28 degrees; dose sensitivity, response rate, and maximal output were affected. Results were similar for sea turtle LH, snapping turtle LH, and ovine follicle-stimulating hormone. Thus, the temperature dependence of the two endocrine systems may have a different rate-limiting component.