Release Of Melanophore-stimulating Hormone Research Articles

Key Factors Influencing Juvenile Quality In Mariculture: A Review

Environmental (temperature, salinity) and nutritional (DHA, EPA, ArA, vitamin A, phospholipids, iodine) factors during larvae rearing largely dictate the successful transformation of larvae to juveniles during metamorphosis which, in turn, determines juvenile quality. Studies on Atlantic halibut, turbot and Japanese flounder report higher metamorphic success, in terms of pigmen- tation, eye migration and general development, when copepods, rather than enriched Artemia, were fed to larvae. Copepods have higher levels of vitamin A, which is required for the synthe- sis of rhodopsin in the retina, a critical visual pigment in the rods necessary for vision at low light intensities. Deficient rhodopsin affects neural transmission from the retina via the central nervous system that triggers pituitary production of melanophore stimulating hormone leading to reduced melanin synthesis and pigmentation deficiency. DHA, an abundant PUFA in copepods, is also vital to vision as it provides the membrane fluidity necessary for rhodopsin to function when stim- ulated by light. The essential fatty acids EPA and ArA are more involved in eicosanoid synthe- sis. These highly potent metabolites are thought to regulate the mechanisms involved in the release of melanophore stimulating hormone and pigmentation. Thyroid hormones play a major role in regulating many developmental processes that occur during metamorphosis. Immersing different age marine fish larvae into various concentrations of thyroid hormone has been shown to synchronize and shorten the duration of metamorphosis in a dose dependent manner in species such as grouper. However, the effect of this immersion on survival varied with the type of thyroid hormone, dose and timing of application. In some species, such as the European seabass (Dicentrarchus labrax), females grow up to 40% faster than males. However, when this species is intensively cultured, masculinization can result in a 70-90% male population. A num- ber of studies have shown that manipulating temperature and salinity during larviculture can result in higher quality juveniles, i.e., a higher percent of faster growing females.

Assessment of TRH as a potential MSH release stimulating factor in Xenopus laevis

This study considers the possible involvement of the tripeptide TRH (thyrotropin releasing hormone) in the physiological regulation of melanophore stimulating hormone (MSH) secretion from the pars intermedia of the toad, Xenopus laevis. TRH was shown to stimulate release of MSH from superfused neurointermediate lobes obtained from white-background adapted animals, but had no effect on secretion from lobes of black-background adapted animals. Immunohistochemical analysis revealed a rich TRH-containing neuronal network terminating in the neural lobe of the Xenopus pituitary. Plasma levels of TRH, determined with a specific radioimmunoassay, proved to be extremely high and no significant difference in this level could be found between white- and black-adapted animals. Plasma TRH probably originates from the skin, and our results show that its concentration is within the effective concentration range established for this peptide in stimulating MSH release from the pars intermedia. Therefore, while both our superfusion and immunohistochemical results argue favourably for a function of TRH in the regulation of MSH secretion, we conclude that, in any regulatory role, it would likely have to function within the pars intermedia at concentrations exceeding the high plasma values. While TRH could be involved in short-term activation of the secretory process in white-background adapted animals or in animals undergoing the initial stages of black background adaptation, our results indicate that this peptide may have no function in the maintenance of secretion from the pars intermedia of animals fully adapted to black background.

GABA and Dopamine Act Directly on Melanotropes of Xenopus to inhibit MSH secretion

The release of melanophore stimulating hormone (MSH) from the pars intermedia of the amphibian Xenopus laevis is regulated by multiple factors of hypothalamic origin. The aim of this study was to determine if potential secretagogues function through a direct action on the melanotrope cell. For this purpose an in vitro superfusion system containing isolated melanotropes (cell suspension) was utilized. The viability of the cells in suspension was tested by examining their ability to synthesize, process and release pro-opiomelanocortin (POMC) related peptides. All biosynthetic functions appeared normal, with the exception that the isolated melanotropes are unable to N-terminally acetylate MSH. Release of immunoreactive-MSH from these cells was shown to be Ca 2+-dependent and high K + stimulated release. Both the neurotransmitters dopamine and γ-aminobuiyric acid (GABA), which are thought to be physiologically important MSH-release inhibiting factors, were shown to inhibit MSH release from isolated melanotropes. Dopamine appeared to function through a dopamine D2 type receptor mechanism while for GABA, both a GABAa and GABAb receptor mechanism are involved.

Regulation of melanotropin release from the pars intermedia of the amphibian Xenopus laevis: Evaluation of the involvement of serotonergic, cholinergic, or adrenergic receptor mechanisms

Melanophore-stimulating hormone (MSH) release from the pars intermedia of the pituitary gland is probably regulated by multiple factors of hypothalamic origin. We have examined a number of potential regulatory factors for their effects on MSH release from the amphibian Xenopus laevis. Serotonin and acetylcholine have no effect on MSH release. Both adrenaline and noradrenaline inhibit release of MSH in a dose-dependent manner. Studies with specific receptor agonists and antagonists reveal that these neurotransmitters exert their in vitro effects primarily through a dopamine D-2 receptor, although and α-adrenergic receptor could not be excluded. We further conclude that the pars intermedia of X. laevis lacks a β-adrenergic receptor for the regulation of MSH secretion from the pars intermedia. In mammals, this receptor activates the adenylate cyclase system. Our studies reveal that despite the lack of β-adrenergic receptors, cyclic-AMP is likely an intracellular factor involved in the stimulation of MSH release.

Secretory activity of the intraocular homotransplanted pars intermedia of the frog, Rana nigromaculata.

To examine whether there is a possible inhibitory effect of melanophore-stimulating hormone (MSH) on the release of MSH from the pars intermedia, two groups of frogs, Rana nigromaculata, were prepared with median eminence extirpation to eliminate the inhibitory hypothalamic control over MSH secretion. In one of the two groups, the animal's own intermediate lobe was transplanted to the anterior chamber of the eye (intraocular autotransplanted gland), and in the second, the animal's own pars intermedia was left in situ, and another pars intermedia was homotransplanted intraocularly. The MSH content of the homotransplanted pars intermedia was usually much increased and the number of secretory granules augmented in the secretory cells in comparison with the autotransplanted gland. These results lead to the conclusion that the release of MSH from the intraocular pars intermedia is inhibited by the in situ pars intermedia of host animals and indicate that MSH acts directly at the pituitary level to inhibit its further release, thus supporting the concept of mass action-type feedback control.

The hypothalamo-hypophyseal rat explant in vitro: endocrinological studies of the pars intermedia dopaminergic neural input.

Short-term in vitro incubation of hypothalamo-hypophyseal tissue from young rats was undertaken to discern more clearly the functional relationship between putative dopaminergic neural projections in the pars intermedia and the secretory activity of melanophore stimulating hormone (MSH). This explant consisted of a portion of the mediobasal hypothalamus containing the dopamine neurone cell bodies of interest, with the attached pituitary neuro-intermediate lobe (n.i.l.). The n.i.l. was inserted into the end of a 1 mm diameter tube attached to a perfusion pump which allowed uninterrupted sampling of medium neighbouring the n.i.l. A 'real-time' analysis of hormone secretion was obtained by immediately and continuously bioassaying for MSH. A bipolar stimulating electrode was placed on the ventral floor of the mediobasal hypothalamus either directly on the arcuate nucleus, median eminence or infundibular stalk. Electrical stimulation for 5 min (0.1-20.0 Hz) caused a transient inhibition of basal MSH secretion, while continuous stimulation (0.1-5.0 Hz) led to a much greater, long-term, reversible inhibition. In the latter, the degree of inhibition was generally dependent on stimulation rate up to a maximum at 5 Hz. Application of the dopamine D2 receptor antagonist, 1-sulpiride (0.001-0.1 microM) to the perfusion medium not only completely and reversibly blocked the stimulus-induced inhibition of MSH release but by itself, significantly increased the basal secretion rate. Applied to the isolated n.i.l., 1-sulpiride did not alter release but did prevent the inhibitory response caused by exogenously applied dopamine (0.1 microM). The gamma-aminobutyric acid receptor antagonist, bicuculline (0.01-1.0 microM), had no effect on any of the parameters studied. In explants, cutting the infundibular stalk linking the mediobasal hypothalamus with the n.i.l., mimicked the effects of 1-sulpiride by interrupting impulse flow to the gland. Thus, electrical stimulation of hypothalamic neurones in these explants apparently causes a release of dopamine from nerve terminals in the pars intermedia to inhibit MSH secretion and perhaps other pro-opiomelanocortin-derived peptides as well.

Neurohypophysial Peptides and the Regulation of Melanophore Stimulating Hormone (MSH) Secretion

Melanophore stimulating hormone (MSH) secretion from the vertebrate pars intermedia is regulated as for other pituitary hormones, by the hypothalamus. Removal of the pituitary from hypothalamic control results in an autonomous uninhibited secretion of MSH. Thus, as for prolactin, the hypothalamus exerts a tonic inhibitory control over MSH secretion. The nature of this inhibitory mechanism is presently being debated with two general models being considered. It is suggested by some investigators that peptides of neurohypophysial hormone origin act as MSH releasing and inhibiting factors (MRF' and MIF's, respectively). In this scheme, the neurohypophysial hormones such as oxytocin would serve as prohormones which by enzymatic cleavage by hypothalamic enzymes would yield MSH releasing and/or inhibiting factors. It is suggested that the terminal tripeptide side chain is an MIF whereas the N-terminal pentapeptide sequence of oxytocin is an MRF. The data supporting this hypothesis comes from work of a few investigators that espouse this scheme. To our knowledge, the so-called MSH releasing and inhibiting factors have proven ineffective in the hands of all other investigators in regulating MSH release.

Synthesis, storage, and release of MSH in the pars intermedia of the pituitary gland of Xenopus laevis during background adaptation

Pituitary levels of melanophore-stimulating hormone (MSH), release of MSH, and protein synthetic activity in the pars intermedia were determined in Xenopus laevis during background adaptation. MSH was measured using a radioimmunoassay to α-MSH; uptake of [3H]lysine, determined autoradiographically, was used to assess protein synthesis; changes in melanophore index indicated changes in release of MSH. Adaptation to black background led to eventual depletion of MSH and increased protein synthetic activity. Conversely, during adaptation to a white background MSH levels increased and protein synthesis decreased. Changes in synthesis lagged considerably behind changes in release. During the initial stage of black-background adaptation, release of MSH was not accompanied by simultaneous decrease in levels of MSH in the gland from which it is concluded that replenishment of MSH took place. Our results indicated that this replenishment in the gland could not be accounted for by de novo synthesis of the hormone. It is proposed that a stored precursor to MSH exists, conversion of which provides for rapid replenishment of MSH. It is suggested that the factor(s) controlling MSH release affect synthesis of this hormone only indirectly.

Metabolic requirements for melanophore-stimulating hormone (MSH) secretion

Melanophore-stimulating hormone (MSH) secretion is regulated by an active transport (Na +−K + pump) system. Release of MSH in vitro from the frog or rat pars intermedia is acutely sensitive to any physiological changes affecting the substrates for active transport. Addition of glucose to the incubation medium, for example, reversibly enhances MSH secretion over that of medium lacking the sugar. Dinitrophenol, cyanide, oligomycin, deoxyglucose, and iodoacetic acid reversibly inhibit MSH secretion, suggesting citric acid cycle and glycolytic pathway contributions to MSH secretion. Oligomycin is the most potent inhibitor of MSH release suggesting that high-energy intermediates may be final important factors in MSH release. The effects of these metabolic inhibitors are antagonized by the presence of glucose in the incubation medium. Cytochalasin B is inhibitory to MSH secretion and its effect is antagonized in medium containing glucose, suggesting that its mechanism of action also may relate to effects on active transport. Cold temperature is reversibly inhibitory to MSH release. The unique feature of the pars intermedia cell in vitro is its acute energy requirement needed to maintain continuous active transport function for the secretion of MSH.

Cellular mechanisms controlling melanophore stimulating hormone (MSH) release

Melanophore stimulating hormone (MSH) release from the vertebrate pars intermedia is under an inhibitory control by the hypothalamus. Catecholamines both inhibit and stimulate MSH release from the isolated frog neurointermediate lobe or rat (and mouse) pituitary. Classical pharmacological methods using specific adrenergic receptor agonists and antagonists reveal that inhibition of MSH release by catecholamines is mediated through either alpha adrenergic receptors and/or dopamine receptors whereas stimulation of MSH release by catecholamines is mediated through beta adrenergic receptors. These results provide the physiological correlate for the morphological evidence of pars intermedia regulation by direct neuronal innervation. Acetylcholine also stimulates MSH release from the frog neurointermediate lobe and this enhanced hormone secretion is mediated through cholinergic receptors (blocked by atrophine, but not by propranolol). The possible interactions of adrenergic and cholinergic receptor mechanisms in the control of MSH release is still to be determined. Neither boiled nor acid-treated hypothalamic extracts inhibit or stimulate MSH release in vitro thus failing to implicate (by these methods) hypothalamic inhibiting or stimulating factors, if present, in the control of MSH release. Our in vitro experiments also fail to support a so-called “auto-feedback” (mass action) regulation of MSH release in either the rat, the frog, or the toad. Numerous similarities between the mechanisms involved in the control of MSH and prolactin release are apparent.

Melanophore stimulating hormone (MSH) release: inhibition by cytochalasin B and "stimulation" by dimethyl sulfoxide.

Incubation of rat or frog pituitaries in cytochalasin B (10-4 minus 10-8 g/ml) for 2, 4 or 6 hr produces a time-dependent inhibition of MSH release. This inhibition is reversible and, again, time-dependent since longer incubations of pituitaries returned to normal media result in greater hormone secretion. Cytochalasin B inhibits MSH release even at a high concentration (10%) of dimethylsulfoxide (DMSO) which, itself, is "stimulatory" to hormone release. MSH release in high DMSO concentration is also inhibited by ouabain or by the absence of Ca2+ from the medium. In amphibian Ringer enriched with glucose, and in Medium 199, cytochalasin B fails to inhibit the release of MSH from the frog pituitary. Colchicine, vinblastine, and vincristine (10-3 minus 10-6 g/ml) were without effect on MSH release. These data suggest a possible role for microfilaments in the control of MSH release but fail to provide information on the exact nature of the mechanisms involved.

The effect of apomorphine and ergocriptine on the release of MSH by the pars intermedia of Rana pipiens.

In an attempt to further characterize the nature of the innervation controlling melanophore-stimulating hormone (MSH) release from the pars intermedia (PI), pellets containing either apomorphine or ergocriptine were implanted in contact with the PI of the frog, and the effect on the animal's coloration was observed. Frogs with apomorphine implants exhibited skin pallor for several hours and those with ergocriptine implants were pallid for a few days. Hypophysectomized (HX) frogs which had been darkened with MSH regained their pallor no sooner when given an injection of apomorphine than with the vehicle. However, intact dark frogs lightened when injected with apomorphine. Frogs darkened by autotransplantation of the PI to the dorsal lymph sac were lightened by an injection of apomorphine. Frogs lightened by an ergocriptine implant on the PI and then darkened by MSH did not lighten sooner than HX frogs given an injection of MSH. Ergocriptine-containing pellets implanted in the thigh took longer to produce the same effect than those implanted in contact with the PI. Since apomorphine is known to stimulate dopamine receptors in the central nervous system, and there is some evidence that ergocriptine does also, the above evidence supports the hypothesis that dopamine receptors are present in the PI.

An investigation of the neural mechanisms controlling the colour change responses of the dogfish, Scyliorhinus canicula L. by mesencephalic and diencephalic lesions

Small, central and bilateral electrolytic lesions and cuts were placed in the mesencephalon and diencephalon of the dogfish ( Scyliorhinus canicula ) to locate the areas involved in the inhibitory control of release of melanophore-stimulating hormone from the neurointermediate lobe of the pituitary. A mid-line hypothalamic tract was demonstrated from the region of the nucleus medius hypothalamicus (n. m. h.) to the neurointermediate lobe; section of this tract led to darkening of the fish. This system is thought to be aminergic. Ablations of the pre-optic nucleus or ‘classical’ neurosecretory tracts anterior to this system were without effect on colour change as were lesions in the more lateral regions of the hypothalamus involving the nuclei lobi inferiores (n. l. i.). In the posterior thalamus bilateral areas immediately anterior to the recessus posterior were shown to be involved in the mechanisms controlling melanophore-stimulating hormone release. Damage to the optic system, including optic nerves, ascending tractus opticus or tectum also produced a darkening response. The neuronal connexions from the optic system to the thalamus or hypothalamus were not located though the bilateral thalamic region may link anteriorly with the n. m. h. Ultrastructural observations of the n. m. h. and n. l. i. demonstrated that both nuclei are composed of neurons containing dense-cored vesicles of 90 nm diameter, thought to be carriers of amines. Somatic-synapses, containing similar vesicles, were present on the cells of both nuclei; thus there may be another aminergic component, associated with the n. m. h., in the colour change mechanisms.

Biogenic amines and control of melanophore stimulating hormone release.

Release of melanophore stimulating hormone (MSH) from the vertebrate pars intermedia is under inhibitory control by the hypothalamus. Removal of the rat pituitary or the neurointermediate lobe of the frog (Rana pipiens) to in vitro incubation medium results in rapid uninhibited release of MSH. This secretion is inhibited by norepinephrine, epinephrine, phenylephrine, and dopamine, and the inhibition is antagonized by alpha-adrenergic receptor blocking agents. Isoproterenol stimulation of MSH secretion from isolated glands is blocked by pro-pranolol, a beta-adrenergic receptor antagonist. These results implicate dopaminergic or classical alpha-adrenergic receptors (or both) in inhibition of MSH release by catecholamines, and implicate beta-adrenergic receptors in stimulation of MSH release by the bioamines.

Melanophore Responses and Intermediatelobe Activity in the Eel Anguilla anguilla after Injection of 6‐OH‐dopamine

AbstractWhen 6‐OH dopamine (6‐OHDA) was injected into the body cavity of eels (Anguilla anguilla L.), which had been kept on a light background with continuous artificial illumination or a natural day‐night regime in May and June, evident but heterogeneous chromatic reactions were induced. After peripheral drug effects during the first 6 hours, the eels became darker for 2 or 3 days, whereupon the melanophore index (MI), in most cases, decreased. Darkening was accompanied by significant nuclear hypertrophy and moderate degranulation of the MSH (melanophore‐stimulating hormone) cells. Probably only some of the adrenergic nerves in the neural lobe were affected. The blood supply to the brain was decreased for several days after each injection. The results support the assumption that in the eel catecholamines released from nerve endings in the neural lobe inhibit the release of MSH from intermedia cells by their own action as an inhibiting factor, or by affecting an MIF (MSH‐release inhibiting factor) and/or an MRF (MSH‐releasing factor).

Ionic requirements for melanophore-stimulating hormone (MSH) release

In vitro studies on ionic requirements for melanophore-stimulating hormone (MSH) release were carried out on a variety of vertebrate species. Frog ( Rana pipiens, Agalychnis dacnicolor), toad ( Bufo marinus), lizard ( Anolis carolinensis), mouse, and rat pituitaries release an MSH-like substance into the incubation medium. incubation of the separated pars distalis or pars intermedia of the frog or rat reveal that most MSH-like activity is confined to the intermediate lobe, suggesting that the hormone is MSH. Removal of the Ca 2+ ion from the medium results in an almost total inhibition of MSH release from the pituitary of each of the species studied. Similarly, removal of the K + ion reduces secretion to about half that of control values, except in the mouse and the toad ( B. marinus), where such an effect could not be demonstrated. High (5×) K + failed to increase the rate of MSH release in either normal or Ca 2+-deficient media. Long-term (4–8 hr) incubation of frog or rat pituitaries in a Ca 2+-deficient medium did not decrease the level of pituitary MSH over that of pituitaries incubated for similar lengths of time in normal media. Excess (10×) Ca 2+ failed to stimulate MSH release from frog or rat pituitaries over that released into normal media. Ouabain reversibly blocked the release of MSH from frog ( R. pipiens) and rat pituitaries. Ouabain failed to block MSH release from the mouse and the toad, B. marinus (the two species which were similarly unresponsive to the absence of K + from the medium). MSH release from the frog was inhibited in a Li +-Ringer or an isotonic sucrose medium. These results suggest that MSH release from pars intermedia cells may be regulated by a Na +K + pump (active transport) mechanism. Although Ca 2+ is ultimately necessary for MSH release (in all species studied), its role may be secondary to that of an initial action of MSH release-inhibiting factors on cellular permeability to the K + and/or Na + ion. The experimental evidence presently suggests that some species may not possess an active transport system linked to the Ca 2+ ion requirement for hormone release.

Melanophore stimulating hormone: release inhibition by ring structures of neurohypophysial hormones.

Tocinamide and tocinoic acid, ring structures of oxytocin, are potent inhibitors of the release of melanophore stimulating hormone from the rat and hamster pituitary in vitro. Tocinamide is effective at concentrations as low as 10-(14)M on the mammalian pituitary. These peptides do not affect release of the hormone on the frog (Rana pipiens) pars intermedia, but they do inhibit release in the bullfrog (Rana catesbeiana) and the toad (Bufo marinus). The specificity of the peptides on inhibition of the hormone is demonstrated by the fact that oxytocin, lysine vasopressin, and pressinoic acid and pressinamide (ring structures of the vasopressins) do not show such inhibitory activity. Hypothalamic extracts of either the frog (Rana pipiens) or the rat inhibit release of the hormone from pituitaries of either species. The inhibitory effects of tocinamide and tocinoic acid, like that of hypothalamic extracts, are reversible.

The amount of melanophore-stimulating hormone in single pituitary glands of Xenopus laevis kept under various conditions

The MSH (melanophore-stimulating hormone) content of single anterior and intermediate/posterior pituitary lobes of Xenopus laevis was determined using skin pieces of Anolis carolinensis as test objects. Significant changes in the MSH content of single intermediate/posterior lobes of Xenopus were found after adaptation during a 48 hour period to a black or to a white background. The ratios of the pigment-stimulating potencies of anterior to intermediate/posterior pituitary lobes are about 1:38 for white background-adapted Xenopus, and about 1:9 for black background-adapted animals. The results of the experiments indicate that under the given adaptation conditions the release of MSH is inhibited in white background-adapted Xenopus and the hormone stored in the pituitary. The hormone is continuously released in black background-adapted animals. Exposure to complete darkness does not deprive the pituitary of Xenopus laevis or that of Rana temporaria of its MSH.