PMID- 31388597

OWN - NLM
STAT- PubMed-not-MEDLINE
LR - 20190807
IS - 2451-8301 (Electronic)
IS - 2451-8301 (Linking)
VI - 7
DP - 2019 Dec
TI - Hippocampal neurons in direct contact with astrocytes exposed to amyloid
beta25-35 exhibit reduced excitatory synaptic transmission.
PG - 34-41
LID - 10.1016/j.ibror.2019.07.1719 [doi]
AB - Amyloid beta protein (Abeta) is closely related to the progression of
Alzheimer's
disease because senile plaques consisting of Abeta 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
Abeta
fragment 25-35 (Abeta25-35) affect synaptic transmission. We show that
synaptic
transmission by hippocampal neurons was inhibited by astrocytes exposed to
Abeta25-35. The Abeta25-35-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 Abeta25-35-exposed
astrocytes and hippocampal neurons. These data indicate that direct contact
between Abeta25-35-exposed astrocytes and neurons is critical for inhibiting
synaptic transmission in the progression of Alzheimer's disease.
FAU - Oyabu, Kohei
AU - Oyabu K
AD - Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka
University, Fukuoka, Japan.
FAU - Kiyota, Hiroki
AU - Kiyota H
AD - Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka
University, Fukuoka, Japan.
FAU - Kubota, Kaori
AU - Kubota K
AD - Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka
University, Fukuoka, Japan.
AD - A.I.G. Collaborative Research Institute for Aging and Brain Sciences, Fukuoka
University, Fukuoka, Japan.
FAU - Watanabe, Takuya
AU - Watanabe T
AD - Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka
University, Fukuoka, Japan.
AD - A.I.G. Collaborative Research Institute for Aging and Brain Sciences, Fukuoka
University, Fukuoka, Japan.
FAU - Katsurabayashi, Shutaro
AU - Katsurabayashi S
AD - Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka
University, Fukuoka, Japan.
FAU - Iwasaki, Katsunori
AU - Iwasaki K
AD - Department of Neuropharmacology, Faculty of Pharmaceutical Sciences, Fukuoka
University, Fukuoka, Japan.
AD - A.I.G. Collaborative Research Institute for Aging and Brain Sciences, Fukuoka
University, Fukuoka, Japan.
LA - eng
PT - Journal Article
DEP - 20190723
PL - England
TA - IBRO Rep
JT - IBRO reports
JID - 101691215
PMC - PMC6669318
OTO - NOTNLM
OT - Alzheimer's disease
OT - Astrocytes
OT - Abeta
OT - Synaptic release
EDAT- 2019/08/08 06:00
MHDA- 2019/08/08 06:01
CRDT- 2019/08/08 06:00
PHST- 2019/05/23 00:00 [received]
PHST- 2019/07/16 00:00 [accepted]
PHST- 2019/08/08 06:00 [entrez]
PHST- 2019/08/08 06:00 [pubmed]
PHST- 2019/08/08 06:01 [medline]
AID - 10.1016/j.ibror.2019.07.1719 [doi]
AID - S2451-8301(19)31771-6 [pii]
PST - epublish
SO - IBRO Rep. 2019 Jul 23;7:34-41. doi: 10.1016/j.ibror.2019.07.1719. eCollection
2019 Dec.