Kuribara M et al. (2011), Brain-derived neurotrophic factor stimulates gr...

XB-ART-42114

Gen Comp Endocrinol 2011 Jan 01;1701:156-61. doi: 10.1016/j.ygcen.2010.09.020.

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Brain-derived neurotrophic factor stimulates growth of pituitary melanotrope cells in an autocrine way.

Kuribara M , Hess MW , Cazorla M , Roubos EW , Scheenen WJ , Jenks BG .

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Brain-derived neurotrophic factor (BDNF) is expressed in the mammalian pituitary gland, in both the anterior and intermediate lobes, where its functional significance is unknown. Melanotrope cells in the intermediate pituitary lobe of the amphibian Xenopus laevis also produce BDNF, which co-exists in secretory granules with α-melanophore-stimulating hormone (α-MSH), a peptide that causes pigment dispersion in dermal melanophores during adaptation of the toad to a dark background. Xenopus melanotropes are highly plastic, undergoing very strong growth to support the high biosynthesis and release of α-MSH in black-adapted animals. In this study we have tested our hypothesis that this enhanced growth of the melanotrope is maintained by autocrine release of BDNF. Furthermore, since the extracellular-regulated kinase (ERK) pathway is a major component of BDNF signaling in neuronal plasticity, we investigated its involvement in melanotrope cell growth. For these purposes melanotropes were treated for 3 days in vitro, with either an anti-BDNF serum or a recombinant tropomyosin-receptor kinase B (TrkB) receptor fragment to eliminate released BDNF, or with the ERK inhibitor U0126. We also applied a novel inhibitor of the TrkB receptor, cyclotraxin-B, to test this receptor's involvement in melanotrope cell growth regulation. All treatments markedly reduced melanotrope cell growth. Therefore, we conclude that autocrine release of BDNF and subsequent TrkB-dependent ERK-mediated signaling is important for melanotrope cell growth during its physiologically induced activation.

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Species referenced: Xenopus laevis
Genes referenced: bdnf mapk1 ntrk2

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	Fig. 1. Alignment of amino acid sequences of preproBDNF from human and Xenopus laevis. The putative signal sequence and the sequence of mature BDNF is marked as first highlight and second highlight respectively. The sequence of cyclotraxin-B and its match in Xenopus laevis is indicated with a frame. ∗ = homologous sequence; : = conserved substitution site; and . = semi-conserved substitution site.
	Fig. 2. Average cell diameters in μm + S.E.M. of melanotrope cells from black-adapted animals, incubated for 3 days in complete XL15 containing (a) normal rabbit IgG (control) or anti-BDNF serum, and (b) normal rabbit IgG (control) or 100 ng/ml recombinant BDNF in addition to BDNF-antiserum. Top letters indicate statistically significant difference with respective groups (P < 0.05; n = 3).
	Fig. 3. Average cell diameters in μm + S.E.M. of melanotrope cells from black-adapted animals, incubated for 3 days in complete XL15 containing 10% PBS (control), with (a) 1 μM recombinant TrkB-fragment in PBS (Fc-TrkB chimera), or with (b) 100 ng/ml recombinant BDNF in addition to recombinant TrkB-fragment. Top letters indicate statistically significant difference with respective groups (P < 0.05; n = 3).
	Fig. 4. Average cell diameters in μm + S.E.M. of melanotrope cells from black-adapted animals, incubated for 3 days in XL15 (control), or 100 μM cyclotraxin-B. Top letters indicate statistically significant difference with respective groups (P < 0.05; n = 3).
	Fig. 5. Average cell diameters in μm + S.E.M. of melanotrope cells from black-adapted animals, during 3 days incubation in XL15, showing the inhibitory effect of 100 μM U0126. Top letters indicate statistically significant difference with respective groups (P < 0.05; n = 3).