In vivo administration of granulocyte colony-stimulating factor restores long-term depression in hippocampal slices prepared from transgenic APP/PS1 mice
Article first published online: 24 MAR 2014
© 2014 Wiley Periodicals, Inc.
Journal of Neuroscience Research
Volume 92, Issue 8, pages 975–980, August 2014
How to Cite
Song, S., Wang, X., Sava, V., Weeber, E. J. and Sanchez-Ramos, J. (2014), In vivo administration of granulocyte colony-stimulating factor restores long-term depression in hippocampal slices prepared from transgenic APP/PS1 mice. J. Neurosci. Res., 92: 975–980. doi: 10.1002/jnr.23378
- Issue published online: 13 JUN 2014
- Article first published online: 24 MAR 2014
- Manuscript Accepted: 18 FEB 2014
- Manuscript Revised: 24 DEC 2013
- Manuscript Received: 25 SEP 2013
- U.S. Department of Veterans Affairs
- USF-Byrd Alzheimer Center
- hematopoietic growth factor
Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic cytokine that also possesses neurotrophic and antiapoptotic properties. G-CSF has been reported to decrease amyloid burden significantly, promote hippocampal neurogenesis, and improve spatial learning in a mouse model of Alzheimer's disease. To understand better the effects of G-CSF on hippocampal-dependent learning, the present study focused on electrophysiological correlates of neuroplasticity, long-term potentiation (LTP), and long-term depression (LTD). Two cohorts of transgenic APP/PS1 mice, with or without prior bone marrow transplantation from Tg GFP mice, were treated in vivo for 2 weeks with G-CSF or vehicle. After completion of the treatments, hippocampal slices were prepared for electrophysiological studies of LTP and LTD. LTP was induced and maintained in both G-CSF-treated and vehicle-treated groups of Tg APP/PS1. In contrast, LTD could not be induced in vehicle-treated Tg APP/PS1 mice, but G-CSF treatment restored LTD. The LTP and LTD results obtained from the cohort of bone marrow-grafted Tg APP/PS1 mice did not differ from those from nongrafted Tg APP/PS1 mice. The mechanism by which G-CSF restores LTD is not known, but it is possible that its capacity to reduce amyloid plaques results in increased soluble oligomers of amyloid-β (A-β), which in turn may facilitate LTD. This mechanism would be consistent with the recent report that soluble A-β oligomers promote LTD in hippocampal slices. © 2014 Wiley Periodicals, Inc.