New aspects of signal transduction in the Xenopus laevis melanotrope cell

Roubos, Eric W.; Scheenen, Wim J.J.M.; Cruijsen, Peter M. J. M.; Cornelisse, L. Niels; Leenders, H.J.; Jenks, Bruce G.

doi:10.1016/s0016-6480(02)00013-8

Cited by 18 publications

(19 citation statements)

References 36 publications

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“…Within the pars intermedia there is a sparse fiber network containing noradenaline [17] and/or serotonin [18]; both transmitters stimulate α-MSH secretion, noradrenaline acting via the β-adrenergic receptor [19]. Nerve terminals in the pars nervosa are the source of a number of stimulatory neuropeptides including TRH [20], corticotropin-releasing hormone (CRH) [21] and more recently the CRH-related peptide urocortin 1 (Ucn 1) has been added to the repertoire of neural lobe peptides that stimulate α-MSH release from the melanotrope cells [22].…”

Section: The Xenopus Neuroendocrine Interface: An Overviewmentioning

confidence: 99%

Plasticity in the Melanotrope Neuroendocrine Interface of Xenopus laevis

Jenks¹,

Kidane²,

Scheenen³

et al. 2007

Neuroendocrinology

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Melanotrope cells of the amphibian pituitary pars intermedia produce α-melanophore-stimulating hormone (α-MSH), a peptide which causes skin darkening during adaptation to a dark background. The secretory activity of the melanotrope of the South African clawed toad Xenopus laevis is regulated by multiple factors, both classical neurotransmitters and neuropeptides from the brain. This review concerns the plasticity displayed in this intermediate lobe neuroendocrine interface during physiological adaptation to the environment. The plasticity includes dramatic morphological plasticity in both pre- and post-synaptic elements of the interface. Inhibitory neurons in the suprachiasmatic nucleus, designated suprachiasmatic melanotrope-inhibiting neurons (SMINs), possess more and larger synapses on the melanotrope cells in white than in black-background adapted animals; in the latter animals the melanotropes are larger and produce more proopiomelanocortin (POMC), the precursor of α-MSH. On a white background, pre-synaptic SMIN plasticity is reflected by a higher expression of inhibitory neuropeptide Y (NPY) and is closely associated with postsynaptic melanotrope plasticity, namely a higher expression of the NPY Y1 receptor. Interestingly, melanotrope cells in such animals also display higher expression of the receptors for thyrotropin-releasing hormone (TRH) and urocortin 1, two neuropeptides that stimulate α-MSH secretion. Possibly, in white-adapted animals melanotropes are sensitized to neuropeptide stimulation so that, when the toad moves to a black background, they can immediately initiate α-MSH secretion to achieve rapid adaptation to the new background condition. The melanotrope cell also produces brain-derived neurotrophic factor (BDNF), which is co-sequestered with α-MSH in secretory granules within the cells. The neurotrophin seems to control melanotrope cell plasticity in an autocrine way and we speculate that it may also control presynaptic SMIN plasticity.

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Section: The Xenopus Neuroendocrine Interface: An Overviewmentioning

confidence: 99%

Plasticity in the Melanotrope Neuroendocrine Interface of Xenopus laevis

Jenks¹,

Kidane²,

Scheenen³

et al. 2007

Neuroendocrinology

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“…The Xenopus pars intermedia contains about 60,000 melanotrope cells, which are activated when the animal is placed on a black (dark) background and inactivated when the background is white (light) (Roubos et al, 1993, 2002, 2005; Roubos, 1997; Jenks et al, 2003, 2007). The activation of the “black melanotrope” is reflected at the ultrastructural level by a well-developed biosynthetic secretory machinery (rough endoplasmic reticulum and Golgi apparatus) and the presence of newly formed, electron-dense secretory granules (De Rijk et al, 1990b).…”

Section: The Melanotrope Neuroendocrine Transducer Cells Of the Southmentioning

confidence: 99%

“…Retrograde neuronal tract tracing with Fast DiI applied to the pituitary pars intermedia identified labeled neurons in, not only, the SCN but also the LC and RN (Ubink et al, 1999). Whereas the LC produces noradrenalin, which probably stimulates melanotrope cell activity (Verburg-Van Kemenade et al, 1986b; Roubos et al, 2002), it seems likely that the melanotrope cells in the Xenopus pars intermedia are also innervated by a serotonergic network originating from neurons in the RN; this network represented the first anatomically identified stimulatory input to the pars intermedia of this species (Ubink et al, 1999). …”

Section: The Melanotrope Neuroendocrine Transducer Cells Of the Southmentioning

confidence: 99%

About a snail, a toad, and rodents: animal models for adaptation research

Roubos¹

2010

Front. Endocrin.

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Neural adaptation mechanisms have many similarities throughout the animal kingdom, enabling to study fundamentals of human adaptation in selected animal models with experimental approaches that are impossible to apply in man. This will be illustrated by reviewing research on three of such animal models, viz. (1) the egg-laying behavior of a snail, Lymnaea stagnalis: how one neuron type controls behavior, (2) adaptation to the ambient light condition by a toad, Xenopus laevis: how a neuroendocrine cell integrates complex external and neural inputs, and (3) stress, feeding, and depression in rodents: how a neuronal network co-ordinates different but related complex behaviors. Special attention is being paid to the actions of neurochemical messengers, such as neuropeptide Y, urocortin 1, and brain-derived neurotrophic factor. While awaiting new technological developments to study the living human brain at the cellular and molecular levels, continuing progress in the insight in the functioning of human adaptation mechanisms may be expected from neuroendocrine research using invertebrate and vertebrate animal models.

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“…This secretory cell is a suitable cell model for such a study, as it expresses L-type, P/Q-type, N-type and R-type Ca 2+ currents channels [10]and, moreover, possesses a wide variety of G-protein-coupled receptors [11]. Xenopus melanotropes release α-melanophore- stimulating hormone (α-MSH), which causes darkening of the skin [12].…”

Section: Introductionmentioning

confidence: 99%

“…Xenopus melanotropes release α-melanophore- stimulating hormone (α-MSH), which causes darkening of the skin [12]. Some of the receptors, such as the corticotropin-releasing hormone (CRH), muscarinic M1 and β-adrenergic receptors, stimulate this release, whereas others, like the neuropeptide Y (NPY) Y1, GABA A , GABA B and D 2 -receptors, inhibit secretion [11, 13]. Most of these receptors act via G-proteins and modulate the pattern of intracellular Ca 2+ oscillations that drive the cell’s secretory activity and arise from Ca 2+ influx through HVA Ca 2+ channels [12, 14].…”

Section: Introductionmentioning

confidence: 99%

Dopamine D2-Receptor Activation Differentially Inhibits N- and R-Type Ca2+ Channels in Xenopus Melanotrope Cells

Zhang

Jenks²,

Ciccarelli³

et al. 2004

Neuroendocrinology

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Dopamine inhibits pituitary melanotrope cells of the amphibian Xenopus laevis through activation of a dopamine (D₂) receptor that couples to a G_i protein. Activated G_i protein subunits are known to affect voltage-operated Ca²⁺ currents (I_Ca). In the present study we investigated which Ca²⁺ currents are regulated by D₂-receptor activation and which G_i protein subunits are involved. Whole-cell voltage-clamp patch-clamp experiments from holding potentials (HPs) of –80 and –30 mV show that 28.6 and 36.9%, respectively, of the total I_Ca was inhibited by apomorphin, a D₂-receptor agonist. The inhibited current had fast activation and inactivation kinetics. From an HP of –80 mV, inhibition of N-type Ca²⁺ currents with ω-conotoxin GVIA and R-type current by SNX-482 reduced the efficacy of the apomorphin-induced inhibition. From an HP of –30 mV this reduction for ω-conotoxin GVIA was still observed. Blocking L-type current by nifedipine or P/Q-type current by ω-agatoxin IVA did not affect apomorphin-induced inhibition at either HP. Our results imply that D₂-receptor activation inhibits both N- and R-type Ca²⁺ currents. Using a strong depolarizing pre-pulse partially reversed the inhibition of the total current by apomorphin. About 50% of this inhibition was achieved through interaction of Gβ/γ proteins, and this part of the inhibited I_Ca had fast activating and inactivating kinetics. However, the other part of the current inhibited by D₂-receptor activation may proceed through Gα-PKA phosphorylation.

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New aspects of signal transduction in the Xenopus laevis melanotrope cell

Cited by 18 publications

References 36 publications

Plasticity in the Melanotrope Neuroendocrine Interface of <i>Xenopus laevis</i>

Plasticity in the Melanotrope Neuroendocrine Interface of <i>Xenopus laevis</i>

About a snail, a toad, and rodents: animal models for adaptation research

Dopamine D<sub>2</sub>-Receptor Activation Differentially Inhibits N- and R-Type Ca<sup>2+</sup> Channels in <i>Xenopus</i> Melanotrope Cells

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