Hippocampal neurons in direct contact with astrocytes exposed to amyloid β25-35 exhibit reduced excitatory synaptic transmission
Kohei Oyabu,
Hiroki Kiyota,
Kaori Kubota,
Takuya Watanabe,
Shutaro Katsurabayashi,
Katsunori Iwasaki
Affiliations
Kohei Oyabu
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan
Hiroki Kiyota
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan
Kaori Kubota
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan; A.I.G. Collaborative Research Institute for Aging and Brain Sciences, Fukuoka University, Fukuoka, Japan
Takuya Watanabe
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan; A.I.G. Collaborative Research Institute for Aging and Brain Sciences, Fukuoka University, Fukuoka, Japan
Shutaro Katsurabayashi
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan; Corresponding author at: Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan.
Katsunori Iwasaki
Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan; A.I.G. Collaborative Research Institute for Aging and Brain Sciences, Fukuoka University, Fukuoka, Japan
Amyloid β protein (Aβ) is closely related to the progression of Alzheimer's disease because senile plaques consisting of Aβ cause synaptic depression and synaptic abnormalities. In the central nervous system, astrocytes are a major glial cell type that contribute to the modulation of synaptic transmission and synaptogenesis. In this study, we examined whether astrocytes exposed to Aβ fragment 25-35 (Aβ25-35) affect synaptic transmission. We show that synaptic transmission by hippocampal neurons was inhibited by astrocytes exposed to Aβ25-35. The Aβ25-35-exposed astrocytes lowered excitatory postsynaptic release and the size of the readily releasable synaptic pool. The number of excitatory synapses was also reduced. However, the number of excitatory synapses was unchanged unless there was direct contact between Aβ25-35-exposed astrocytes and hippocampal neurons. These data indicate that direct contact between Aβ25-35-exposed astrocytes and neurons is critical for inhibiting synaptic transmission in the progression of Alzheimer’s disease. Keywords: Alzheimer’s disease, Aβ, Astrocytes, Synaptic release
