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

Neuroendocrinology - Tập 85 Số 3 - Trang 177-185 - 2007
Bruce G. Jenks1, Adhanet H. Kidane1, Wim J.J.M. Scheenen1, Eric W. Roubos
1Department of Cellular Animal Physiology, Radboud University Nijmegen, Nijmegen, The Netherlands

Tóm tắt

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 <i>Xenopus laevis</i> 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.

Từ khóa


Tài liệu tham khảo

10.1111%2Fj.1749-6632.1999.tb08664.x

10.1006%2Fgcen.2002.7778

10.1016%2F0016-6480%2882%2990158-7

10.1016%2F0024-3205%2886%2990350-4

10.1016%2F0196-9781%2885%2990322-5

10.1016%2F0361-9230%2886%2990206-6

10.1111%2Fj.1749-6632.1993.tb19710.x

10.1159%2F000124685

10.1016%2F0196-9781%2895%2900049-P

10.1210%2Fendo-120-2-622

10.1210%2Fen.138.1.203

10.1002%2F%28SICI%291096-9861%2819980720%29397%3A1%3C60%3A%3AAID-CNE5%3E3.0.CO%3B2-G

10.1002%2Fcne.903310306

10.1046%2Fj.1365-2826.1999.00311.x

10.1016%2FS0016-6480%2802%2900013-8

10.1016%2F0196-9781%2887%2990167-7

10.1016%2F0196-9781%2887%2990142-2

10.1016%2Fj.brainres.2004.12.056

10.1016%2FS0016-6480%2803%2900120-5

10.1007%2FBF00374530

10.1016%2FS0143-4160%2896%2990038-X

10.1111%2Fj.1365-2826.1994.tb00607.x

10.1111%2Fj.1749-6632.1998.tb10867.x

10.1016%2FS0143-4160%2896%2990023-8

10.1054%2Fceca.1999.0051

10.1016%2FS0006-3495%2801%2975679-2

10.1016%2Fj.ygcen.2004.11.010

10.1111%2Fj.1749-6632.1998.tb10765.x

10.1159%2F000084144

10.1016%2Fj.ygcen.2005.08.006

10.1210%2Fen.137.11.4551

10.1677%2Fjoe.0.0530303

10.1159%2F000122619

10.1016%2F0016-6480%2890%2990089-5

10.1016%2F0016-6480%2883%2990009-6

10.1016%2F0006-291X%2887%2991407-0

10.1677%2Fjoe.0.1590281

10.1111%2Fj.1432-1033.1989.tb14695.x

10.1007%2FBF00313970

10.1016%2F0092-8674%2894%2990296-8

10.1016%2FS0306-4522%2899%2900020-2

10.1210%2Fen.142.5.1950

10.1016%2Fj.neuroscience.2004.06.059

10.1210%2Fen.2005-0108

10.1016%2FS0306-4522%2896%2983020-X

10.1016%2F0306-4522%2893%2990432-F

10.1016%2FS0143-4160%2897%2990010-5

10.1074%2Fjbc.273.40.25686

10.1162%2F089976601300014655

10.1046%2Fj.1365-2826.2002.00838.x

10.1046%2Fj.1365-2826.2002.00849.x

10.1046%2Fj.1432-1033.2002.03152.x

10.1002%2Fcne.20235

10.1196%2Fannals.1327.012

10.1210%2Fen.2002-221074

10.1210%2Fen.137.10.4298

10.1210%2Fen.2003-0014

10.1124%2Fjpet.103.049874

10.1055%2Fs-2005-869519

10.1016%2FS0301-0082%2803%2900019-4

10.1016%2Fj.pneurobio.2005.06.003

10.1523%2FJNEUROSCI.3792-05.2006

10.1210%2Fen.143.4.1337

10.1111%2Fj.1365-2826.2004.01110.x

10.1038%2Fnrn1726