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This study investigates whether thyrotropin-releasing hormone (TRH), alpha-melanocyte-stimulating hormone (alpha-MSH) and N-acetyl beta-endorphin (NAc beta-END), or the thyroid hormones thyroxine (T4) and 3,5,3'-triiodothyronine (T3) are involved in the physiological response to temperature changes in the poikilotherm common carp (CYPRINUS CARPIO). Carps were either subjected to a rapid cold exposure or acclimated over time to three different temperatures. Acute cold exposure did not influence blood plasma alpha-MSH concentrations. Acclimation to 15, 22 or 29 degrees C led to a temperature-dependent increase of both alpha-MSH and NAc beta-END plasma concentrations. Moreover, the in vitro sensitivity to TRH of melanotrope cells (that synthesise these peptides) also correlated positively with ambient temperature. Increased TRH activation stimulated processing of the precursor of alpha-MSH and NAc beta-END, resulting in increased release of both peptides and storage of a surplus of NAc beta-END within melanotropes. Plasma T4 levels were highest in carps acclimated to the intermediate temperature tested, and correlated strongly with hypothalamic TRH content. Plasma T3 levels were unaffected by ambient water temperature. We conclude that ambient water temperature influences the sensitivity of melanotrope cells to TRH in carps. This effect, however, is not due to acute temperature change, but evolves during the acclimation process of carps to a new temperature., (Copyright 2003 S. Karger AG, Basel)

Swimming at 25-30 degrees C for 30 min stimulates release of beta-endorphin from both the anterior and intermediate lobe of the pituitary in rats. Measurement of N-acetyl beta-endorphin-immunoreactivity (IR), which is specific for intermediate lobe secretion, indicates a 2- to 3-fold increase in N-acetyl beta-endorphin IR in plasma following this challenge. When swim is repeated on a daily basis, there is an increase in the amount of N-acetyl beta-endorphin IR released with repeated swim over time. As well as increased response to the swim challenge, these animals demonstrate an increase in the resting plasma levels of N-acetyl beta-endorphin IR and an increase in the intermediate lobe content of N-acetyl beta-endorphin IR. Molecular sieving of plasma from rats which were swum repeatedly demonstrates that this N-acetyl beta-endorphin IR consists of both larger molecular weight N-acetyl beta-endorphin IR, e.g. N-acetyl beta-endorphin1-31 and C-terminally shortened forms, e.g. N-acetyl beta-endorphin1-27. Administration of propranolol (3 mg/kg), a beta-adrenergic antagonist, 30 min before the onset of swim is able to block the intermediate lobe release of N-acetyl beta-endorphin IR with acute swim challenge. However, repeated administration of propranolol in conjunction with repeated swim is not able to block the swim stress-induced increase in plasma N-acetyl beta-endorphin IR or the increase in N-acetyl beta-endorphin IR content of the intermediate lobe. This is not due to decreased sensitivity to propranolol with repeated administration since in rats given chronic propranolol treatment an acute dose of propranolol is still able to block swim stress-induced release of N-acetyl beta-endorphin IR. Similarly, it is not due to a decreased efficacy of this dose of propranolol in rats which were swum chronically.

Hypothalamo-pituitary disconnection (HPD) in the sheep results in a two-fold increase in pituitary intermediate lobe (IL) immunoreactive (ir)-alpha-N-acetylated endorphin (NacEP) and ir-alpha-melanocyte-stimulating hormone (alpha MSH) content. The rise in IL NacEP content is accompanied by a markedly altered pattern of processing, in that NacEP1-27 becomes the dominant molecular species with a complementary fall in Nac alpha-EP and Nac gamma-EP. To determine if these effects reflect the loss of descending dopaminergic neuronal input to the IL, we have chronically treated two groups (n = 4 per group) of normal sheep with the dopamine antagonist haloperidol or the dopamine agonist bromocriptine; a group of HPD sheep were also treated with bromocriptine. Acid extracts of IL were diluted and ir-alpha-MSH and ir-NacEP content determined by radioimmunoassay; aliquots were submitted to reversed-phase HPLC and collected fractions similarly assayed. Bromocriptine lowered ir-NacEP and ir-alpha-MSH by about 30%; on HPLC the ir-NacEP profiles, and perhaps to a lesser extent those for ir-alpha-MSH were qualitatively similar to untreated controls. In contrast, haloperidol increased by about 45% both ir-NacEP and ir-alpha-MSH levels and produced a marked change in the ir-NacEP molecular profile, with NacEP1-27 becoming the predominant molecular form and other species representing only minor components in the chromatogram. In the treated HPD group, bromocriptine partially restored the processing profiles previously observed in HPD animals to those found in untreated intact animals.(ABSTRACT TRUNCATED AT 250 WORDS)

In homozygous (di/di) Brattleboro rats, pro-opiomelanocortin (POMC) synthesis and processing, and the release of its products, is by definition not under the control of hypothalamic arginine vasopressin (AVP) in contrast with normal rats or heterozygote (di/+) littermates. To explore the role of AVP on these parameters, we have compared homozygotes and heterozygotes in terms of POMC mRNA levels, pituitary content of immunoreactive (ir)-ACTH, ir-beta-endorphin (beta-EP), alpha-melanocyte-stimulating hormone (alpha-MSH) and ir-N-acetyl-EP (NacEP), plasma levels of ir-ACTH and ir-beta-EP, and RP-HPLC profiles of the various forms of ir-alpha-MSH and ir-NacEP. Homozygous rats had immeasurably low levels of hypothalamic ir-AVP, in contrast with their heterozygote littermates; hypothalamic ir-corticotropin releasing factor did not differ between strains. No difference between-strains was seen in levels of POMC mRNA; elevated levels of all pituitary peptides, except ir-ACTH, were found in di/di rats; plasma levels of both ir-ACTH and ir-beta-EP were lower in di/di rats; pituitary ir-alpha-MSH RP-HPLC profiles were similar in both strains, but those for ir-NacEP showed a striking increase in Nac alpha-EP in di/di rats. We interpret these data as evidence for decreased degradation/retarded release of POMC products from the di/di anterior pituitary, for increased processing of POMC products to shorter forms in both anterior pituitary and neuro-intermediate lobe, and thus for a role of AVP in the processing of POMC, as well as POMC synthesis and ACTH/beta-EP release.