Zinc-mediated neuronal death is dependent on Trk activation

Morley, Samuel N., Power, John M., Coulson, Elizabeth J. and Bartlett, Perry F. (2007) Zinc-mediated neuronal death is dependent on Trk activation. Experimental Neurology, 205 2: 360-366. doi:10.1016/j.expneurol.2007.02.006

Author Morley, Samuel N.
Power, John M.
Coulson, Elizabeth J.
Bartlett, Perry F.
Title Zinc-mediated neuronal death is dependent on Trk activation
Journal name Experimental Neurology   Check publisher's open access policy
ISSN 0014-4886
Publication date 2007-06
Sub-type Article (original research)
DOI 10.1016/j.expneurol.2007.02.006
Volume 205
Issue 2
Start page 360
End page 366
Total pages 7
Editor Gilman, S.
Goldman, S.
Place of publication Maryland Heights, MO, United States
Publisher Academic Press
Collection year 2008
Language eng
Subject 270106 Cell Development (incl. Cell Division and Apoptosis)
780105 Biological sciences
Formatted abstract
Zinc release is a primary mediator of neuronal death. Here we show that zinc-mediated death of neurons in vitro is dependent on nerve growth factor (NGF) stimulation and does not occur in response to exposure to leukemia inhibitory factor. NGF priming is regulated, not by the traditional neurotrophin death receptor, p75NTR, but by TrkA, in a protein- and mRNA synthesis-dependent manner. Furthermore, Trk signaling promotes raised free intracellular zinc, mediating neuronal death after extracellular application of zinc. Thus, regulators of Trk signaling provide attractive targets for future treatment of zinc-associated neurological diseases, including stroke, epilepsy and brain trauma.
Keyword Zinc
Neuronal survival
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

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Created: Mon, 18 Feb 2008, 17:26:15 EST