Effects of pharmacological agents on the hypothalamus of Rana pipiens in relation to the control of skin melanophores (2023)

Cited by (17)

  • effect of acetylcholine on the electrical and secretory activities of frog pituitary melanotrophs

    1990, Brain Research

    The activity of melanotroph cells of the amphibian pars intermedia is regulated by multiple factors including classical neurotransmitters and neuropeptides. In this study, we have examined the possible involvement of acetylcholine (ACh) in the regulation of electrical and secretory activities of frog pituitary melanotrophs. Electrophysiological recordings were conducted on cultured cells by using the patch-clamp technique in the whole-cell configuration. In parallel, α-MSH release from acutely dispersed pars intermedia cells was studied by means of the perifusion technique. In all cells tested in the current-clamp mode, superfusion with ACh (10−6 M) gave rise to a depolarization associated with an enhanced frequency of action potentials. Administration of ACh (10−6 M) to perifused cells also induced stimulation of α-MSH release. These results indicate that the neurotransmitter ACh exerts a direct stimulatory effect on pituitary melanotrophs. The action of ACh on electrical and secretory activities was mimicked by muscarine (10−5 M), while ACh-induced α-MSH secretion was completely abolished by the muscarinic antagonist atropine (10−6 M). The depolarizing effect of muscarine was suppressed by the specific M1 muscarinic antagonist pirenzepine (10−5 M), indicating the existence of a M1 subtype muscarinic receptor in frog pars intermedia cells. In addition, using a monoclonal antibody against calf muscarinic receptors, we have visualized, by the immunofluorescence technique, the presence of muscarinic receptor-like immunoreactivity in cultured intermediate lobe cells. Electrophysiological recordings showed that nicotine (10−5 M) induces membrane depolarization associated with an increase of the frequency of action potentials. Nicotine (10−7 − 10−4 M) also caused a dose-related stimulation of α-MSH release from perifused pars intermedia cells. Both electrophysiological recordings and perifusion experiments showed that nicotine-induced stimulation of pituitary melanotrophs was not sensitive to various classical nicotinic antagonists including hexamethonium (10−4 M), α-bungarotoxin (10−5 M),d-tubocurarine (10−5 M), dihydro- β-erythroïdine (10−5 M) and toxin F (10−6 M). In addition, the nicotinic agonists cytisine (10−5 M) and 1,1-dimethyl-4-phenylpiperazinium (10−5 M) did not stimulate α-MSH release. In conclusion, the present results show that ACh acts as a neurohormone to stimulate the electrical and secretory activities of frog pars intermedia cells through M1-muscarinic receptors. Our data also suggest the existence, in our model, of a subtype of nicotinic receptors unrelated to identified nicotinic binding sites.

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

    1986, General and Comparative Endocrinology

    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.

  • Changes in formaldehyde-induced fluorescence of the hypothalamus and pars intermedia in the frog, Rana temporaria, following background adaptation

    1982, Brain Research Bulletin

    Adaptation of the frog, Rana temporaria, to a white background for 12 hr has resulted in an intense formaldehyde-induced fluorescence (FIF) in the neurons of the preoptic recess organ (PRO), paraventricular organ (PVO), nucleus infundibularis dorsalis (NID) and their basal processes permitting visualization of the PRO- and PVO-hypophysial tracts that extend into the median eminence (ME) and pars intermedia (PI); the FIF is reduced in all the structures by 3 days. In frogs adapted to a black background, for 12 hr and 3 days, there was a general reduction in the FIF of the PRO neurons and PRO-hypophysial tract. By 12 hr black background adaptation, the PVO/NID neurons and only their adjacent basal processes show FIF which was sharply reduced by 3 days, making the PVO-hypophysial tract undetectable. In the PI fibers the fluorescence was more intense in black-adapted frogs than in white-adapted ones at both the intervals studied. The simultaneous changes in the FIF of the hypothalamic nuclei, tracts and PI suggest that the PRO and PVO/NID neurons participate in PI control through release of neurotransmitter(s) at the axonal ends.

    (Video) Zoo Pathology of Reptiles & Amphibians Dr Tracy S McNamara
  • 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.

  • A relationship between adrenergic blockage and the secretory process in cells of the pars intermedia of the frog Rana pipiens

    1973, General and Comparative Endocrinology

    Frogs (Rana pipiens) adapted to an intermediate state of melanin dispersion were treated with phentolamine and with propranolol in order to block, respectively, alpha and beta adrenergic receptors. Changes in fine structure of the pars intermedia gland cells indicate that adrenergic receptors of both types are involved in the process of MSH release from the pituitary. It is probable that the adrenergic inhibitory control of MSH release in this species is mediated by receptors of the beta type. It is also suggested that alpha adrenergic receptors are involved in the modulation and perhaps facilitation of MSH output.

  • The effect of long-term exposure to an illuminated white background on the MSH content of the pituitary of Xenopus Laevis

    1973, Comparative and General Pharmacology

    • 1.

      1. Experiments with reserpine on Xenopus of different background histories suggest that long-term exposure to a white background leads to a depletion of MSH in the pars intermedia.

    • 2.

      2. A model involving the brain monoamines (serotonin and catecholamines) for the control of the pars intermedia is proposed.

    • 3.

      3. This follows an explanation for the MSH-releasing effect of reserpine observed by various authors.

    • 4.

      4. A possible ACTH-releasing effect of reserpine in Xenopus is also considered.

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    Studies on the Mode of Action of Psoralen Derivatives: II. The Pituitary Adrenal Axis Control of Copper Metabolism and its Response to Psoralens

    Journal of Investigative Dermatology, Volume 32, Issue 6, 1959, pp. 651-659

Copyright © 1966 Published by Elsevier Inc.

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