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In vivo administration of granulocyte colony‐stimulating factor restores long‐term depression in hippocampal slices prepared from transgenic APP/PS1 mice
Author(s) -
Song Shijie,
Wang Xinming,
Sava Vasyl,
Weeber Edwin J.,
SanchezRamos Juan
Publication year - 2014
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23378
Subject(s) - long term potentiation , hippocampal formation , neurogenesis , genetically modified mouse , granulocyte colony stimulating factor , in vivo , hippocampus , neurotrophic factors , amyloid precursor protein , presenilin , synaptic plasticity , chemistry , pharmacology , medicine , endocrinology , transgene , neuroscience , alzheimer's disease , biology , biochemistry , disease , receptor , microbiology and biotechnology , chemotherapy , gene
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.