Long-term control of neuronal excitability by corticosteroid hormones

Abstract

Long-term control of neuronal excitability by corticosteriod hormonesJoëls, M.; Hesen, W.S.; de Kloet, E.R. Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. AbstractAfter a critical survey of current interpretations of superconductivity in (Ba,K)BiO3, we present a quantitative analysis of this system, with emphasis on dependence of the critical temperature on potassium content and on pressure (external or 'chemical'). Adopting a BCS formalism, Cooper-pair formation is assumed not to be phonon-mediated, but to arise from indirect-exchange interactions between conduction electrons via oxygen anions (oxygen valence band), by analogy with previous analyses of cuprate high-T c superconductors. Numerical calculations are carried through with, and without, accounting for shrinkage of the lattice with increasing potassium content. Results for pressure gradients of T c, at varying doping, and T c under pressures up to 20 GPa, are compared with experimental data. Extension of the analysis to the bismuthate Ba(Pb,Bi)O 3 is outlined.

Factors explaining variance in perceived pain in women with fibromyalgia

“…However, our methodology does not allow us to assess the relative importance of sympathetic dysregulation and relative adrenal insufficiency as cortisol and blood pressure responses to buspirone may not be truly independent variables. Corticosteroids may influence sympathetic neuronal excitability, and activity in the sympatho-adrenal system may influence cortisol secretion [52,53]. …”

Competitive interactions between endogenous LTD and LTP in the hippocampus underlie the storage of emotional memories and stress-induced amnesia

“…It is now well-established that CORT produces a dose-and receptor-specific [mineralocorticoid (MR) vs. glucocorticoid (GR)] modulation of the AHP via MR vs. GR receptor activation. Whereas low concentrations of CORT or activation of MR receptors reduces the AHP and enhances LTP, high concentrations of CORT or activation of GR receptors increases the AHP and suppresses LTP (Joels andde Kloet, 1990, 1992;Kerr et al, 1994;Joels et al, 1995;Pavlides et al, 1995;Roberts and Keith, 1995;Hesen and Joels, 1996b;Smriga et al, 1998;Pavlides and McEwen, 1999;Joels, 2001). The receptor-specific opposing actions of glucocorticoids on the AHP may contribute to the complex, and often opposing, effects of acute stress and glucocorticoid administration on memory (Lupien and McEwen, 1997;Sandi et al, 1997;Conrad et al, 1999;de Kloet et al, 1999;Buchanan and Lovallo, 2001;Jameison and Dinan, 2001;Lupien et al, 2002;Roozendaal, 2002Roozendaal, , 2003Cordero et al, 2003;Erickson et al, 2003;Sandi, 2003;Wolf, 2003;Maheu et al, 2004;Wolf et al, 2004;Conrad, 2005;Kuhlmann et al, 2005a,b).…”

Programming of the Hypothalamo–Pituitary–Adrenal Axis: Serotonergic Involvement

“…Glucocorticoids can alter serotoninmediated neurotransmission (Joels et al, 1995;Meijer and De Kloet, 1998) and may directly affect serotonin levels pre-synaptically, in the synaptic cleft, and post-synaptically. Prenatal exposure to sGC has been shown to alter SERT expression in the postnatal rat brain .…”