Distinguishing the Impacts of Inadequate Prey and Vessel Traffic on an Endangered Killer Whale (Orcinus orca) Population

Managing endangered species often involves evaluating the relative impacts of multiple anthropogenic and ecological pressures. This challenge is particularly formidable for cetaceans, which spend the majority of their time underwater. Noninvasive physiological approaches can be especially informative in this regard. We used a combination of fecal thyroid (T3) and glucocorticoid (GC) hormone measures to assess two threats influencing the endangered southern resident killer whales (SRKW; Orcinus orca) that frequent the inland waters of British Columbia, Canada and Washington, U.S.A. Glucocorticoids increase in response to nutritional and psychological stress, whereas thyroid hormone declines in response to nutritional stress but is unaffected by psychological stress. The inadequate prey hypothesis argues that the killer whales have become prey limited due to reductions of their dominant prey, Chinook salmon (Oncorhynchus tshawytscha). The vessel impact hypothesis argues that high numbers of vessels in close proximity to the whales cause disturbance via psychological stress and/or impaired foraging ability. The GC and T3 measures supported the inadequate prey hypothesis. In particular, GC concentrations were negatively correlated with short-term changes in prey availability. Whereas, T3 concentrations varied by date and year in a manner that corresponded with more long-term prey availability. Physiological correlations with prey overshadowed any impacts of vessels since GCs were lowest during the peak in vessel abundance, which also coincided with the peak in salmon availability. Our results suggest that identification and recovery of strategic salmon populations in the SRKW diet are important to effectively promote SRKW recovery

In vitro study of corticotropin-releasing hormone-induced thyrotropin release: ontogeny and inhibition by somatostatin

Recent research has shown that in the chicken important interactions take place between the adrenal and the thyroidal axis both at the central and the peripheral level. In vivo as well as in vitro experiments showed that ovine corticotropin-releasing hormone (oCRH) clearly increases thyrotropin (TSH) secretion in late embryonic and early posthatch chicks. In vivo experiments in older chickens, however, suggested that this response might disappear at a later stage. Therefore we started to study in detail the ontogeny of the TSH releasing activity of oCRH using the in vitro perifusion technique. Several embryonic stages (E14, E16, and E18) as well as posthatch stages (C1, C8, C22, and adult chickens) were included in the study. We also investigated the possible regulatory role of somatostatin (SRIH) in this specific endocrine function of CRH. The perifusion studies show that CRH stimulated the TSH release at all stages tested. The 10 and 100 nM oCRH doses were almost equally effective at the early embryonic stages while in most posthatch stages the higher oCRH dose was significantly more effective than the lower one. The stimulation factor, representative for the relative increase in TSH secretion following oCRH challenge, was high at early embryonic stages and clearly lower in adult animals. This seemed to be related to an age-dependent increase in basal TSH secretion levels. In both embryonic (E19) and posthatch (C8) chicks a pretreatment of the pituitaries with SRIH lowered the sensitivity of the thyrotropes to an oCRH challenge. This effect was more pronounced in the posthatch chicks compared to the embryos. The results show that CRH is capable of stimulating the TSH secretion during the entire life cycle of the chicken and that SRIH may play an important role in the fine-tuning of this response by lowering the sensitivity of the thyrotropes to CRH. (C) 2003 Elsevier Science (USA). All rights reserved.status: publishe

Inhibition and activation of the thyroidal axis by the adrenal axis in vertebrates

Hormones of the adrenal or interrenal axis and stress situations which induce elevated glucocorticoid plasma levels (e.g. handling and starvation), inhibit thyroid function in growing and adult vertebrates. However, data indicate that during foetal and embryonic development (mammals and birds) or during larval growth and metamorphosis (fish and amphibians), the adrenal axis may stimulate thyroid function. Recent findings have provided some information concerning this stimulatory interference of the adrenal axis. In amphibians corticotropin releasing hormone and not thyrotropin releasing hormone is thyrotropic during metamorphosis, thus providing the substrate T4 necessary for T3 production. Other data indicate that the increase in plasma T3 at metamorphic climax may be the result of an inhibition of the T3 degrading activity, rather than stimulation of the T4 into T3 converting activity, and that glucocorticoids may be responsible for this. Also, in the chick embryo glucocorticoids effectively increase plasma T3 concentration by reducing the hepatic T3 degrading activity, whereas corticotropin releasing hormone also induces an elevation in the thyrotropin plasma levels and hence raises T4 concentrations which may function as a substrate for T3 production.status: publishe

Changes of thyrotropin-releasing hormone (TRH) levels in brain regions and pituitary during induced metamorphosis of Ambystoma mexicanum

Axolotls (Ambystoma mexicanum) are neotenic amphibians: they keep larval features during their entire lifetime. However, metamorphosis can be induced by injection of thyroid hormones or thyrotropin (TSH). The role played by thyrotropin-releasing hormone (TRH) in amphibian metamorphosis is not clear, since TRH treatment never succeeded in inducing metamorphosis in amphibian larvae. We studied the changes of TRH and plasma thyroid hormone levels in axolotls during thyroxine (T-4)-induced metamorphosis. TRH levels in skin, hypothalamus, pituitary and extrahypothalamic region of the brain as well as plasma T-4 and triiodothyronine (T-3) levels were measured by radioimmunoassay (RIA). Preliminary data on the expression of TRH receptors in the pituitary of a neotenic and a metamorphosed animal were obtained by in situ hybridisation with an antisense oligonucleotide probe, based on nucleotides 1011 to 1060 of chicken TRH receptor mRNA. In general, TRH RIA showed that hypothalamus, extrahypothalamic region and pituitary contained high TRH levels. During metamorphosis, TRH levels decreased in hypothalamus land extrahypothalamic region) and increased in pituitary; postmetamorphic values did not differ from neotenic controls TRH levels in skin did not change significantly. During metamorphosis. plasma thyroid hormone levels were high, followed by a decrease to premetamorphic values after metamorphosis. Preliminary in situ hybridisation results suggested that the expression of TRH receptors is low in neotenic animals and increases during T-4-induced metamorphosis.status: publishe

Identification of somatostatin receptors controlling growth hormone and thyrotropin secretion in the chicken using receptor subtype-specific agonists

Somatostatin (SRIH) functions as an endocrine mediator in processes such as growth, immune resistance and reproduction. Five SRIH receptors (sstr1-5) have been identified in mammals, where they are expressed in both the brain and peripheral tissues. To study the specific function of each receptor subtype, specific agonists (ag1-5) have been synthesized. The high degree of homology between mammalian and avian SRIH receptors suggests that these agonists might also be used in chickens. In this paper we describe two in vitro protocols (static incubation and perifusion system) to identify the SRIH receptors controlling the secretion of GH and TSH from the chicken pituitary. We found that basal GH or TSH secretion were never affected when SRIH or an agonist (1 muM) were added. SRIH diminished the GH as well as the TSH response to TSH-releasing hormone (TRH; 100 nM) in both systems. Our results have indicated that the SRIH actions at the level of the pituitary are regulated through specific receptor subtypes. In both the static and flow incubations, ag2 lowered the GH response to TRH, whereas stimulated TSH release was diminished by both ag2 and ag5. Ag3 and ag4 tended to increase rather than decrease the responsiveness of both pituitary cell types to TRH in perifusion studies. Our data have indicated that SRIH inhibits chicken pituitary function through sstr2 and sstr5. Only sstr2 seems to be involved in the control of chicken GH release, whereas both sstr2 and sstr5 inhibit induced GH secretion in mammals. The possible stimulatory action of ag3 and ag4 may point towards a species-specific function of sstr3 and sstr4.status: publishe

Hypothalamic control of the thyroidal axis in the chicken: Over the boundaries of the classical hormonal axes

The pituitary gland, occupying a central position in the hypothalamo-pituitary thyroidal axis, produces thyrotropin (TSH), which is known to stimulate the thyroid gland to synthetize and release its products, thyroid hormones. TSH is produced by a specific cell population in the pituitary, the so-called thyrotropes. Their secretory activity is controlled by the hypothalamus, releasing both stimulatory and inhibitory factors that reach the pituitary through a portal system of blood vessels. Based on early experiments in mammals, thyrotropin-releasing hormone (TRH) is generally mentioned as the main stimulator of the thyrotropes. During the past few decades, it has become clear that the hypophysiotropic function of the hypothalamus is more complex, with different hormonal axes interacting with each other. In the chicken, it was found that not only TRH, but also corticotropin-releasing hormone (CRH), the main stimulator of corticotropin release, is a potent stimulator of TSH secretion. Somatostatin (SRIH), a hypothalamic factor known for its inhibitory effect on growth hormone secretion, was demonstrated to blunt the TSH response to TRH and CRH. In this review we summarize the latest studies concerning the "interaxial" hypothalamic control of TSH release in the chicken, with a special emphasis on the molecular components of these control mechanisms. It remains to be demonstrated if these findings could also be extrapolated to other species or classes of vertebrates. (c) 2005 Elsevier Inc. All rights reserved.status: publishe

Involvement of thyrotropin-releasing hormone receptor, somatostatin receptor subtype 2 and corticotropin-releasing hormone receptor type 1 in the control of chicken thyrotropin secretion

Thyrotropin or thyroid-stimulating hormone (TSH) secretion in the chicken is controlled by several hypothalamic hormones. It is stimulated by thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH), whereas somatostatin (SRIH) exerts an inhibitory effect. In order to determine the mechanism by which these hypothalamic hormones modulate chicken TSH release, we examined the cellular localization of TRH receptors (TRH-R), CRH receptors type I (CRH-R1) and somatostatin subtype 2 receptors (SSTR2) in the chicken pars distalis by in situ hybridization (ISH), combined with immunological staining of thyrotropes. We show that thyrotropes express TRH-Rs and SSTR2s, allowing a direct action of TRH and SRIH at the level of the thyrotropes. CRH-R1 expression is virtually confined to corticotropes, suggesting that CRH-induced adrenocorticotropin release is the result of a direct stimulation of corticotropes, whereas CRH-stimulated TSH release is not directly mediated by the known chicken CRH-R1. Possibly CRH-induced TSH secretion is mediated by a yet unknown type of CRH-R in the chicken. Alternatively, a pro-opiomelanocortin (POMC)-derived peptide, secreted by the corticotropes following CRH stimulation, could act as an activator of TSH secretion in a paracrine way. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.status: publishe