Prevention of age-associated neuronal hyperexcitability with improved learning and attention upon knockout or antagonism of LPAR2.
Aging
Animals
Brain
/ metabolism
Calcium-Binding Proteins
/ deficiency
Chromatography, High Pressure Liquid
Dentate Gyrus
/ metabolism
Discriminant Analysis
EGF Family of Proteins
/ deficiency
Female
Liver
/ metabolism
Long-Term Potentiation
Male
Maze Learning
/ drug effects
Memory
/ drug effects
Mice
Mice, Inbred C57BL
Mice, Knockout
Neurons
/ metabolism
Principal Component Analysis
Receptors, Lysophosphatidic Acid
/ antagonists & inhibitors
Tandem Mass Spectrometry
Cognition
Hippocampal excitability
IntelliCage
Long-term potentiation
Lysophosphatidic acids
Touchscreen
Journal
Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402
Informations de publication
Date de publication:
Feb 2021
Feb 2021
Historique:
received:
13
11
2019
accepted:
13
05
2020
revised:
16
04
2020
pubmed:
30
5
2020
medline:
2
3
2021
entrez:
30
5
2020
Statut:
ppublish
Résumé
Recent studies suggest that synaptic lysophosphatidic acids (LPAs) augment glutamate-dependent cortical excitability and sensory information processing in mice and humans via presynaptic LPAR2 activation. Here, we studied the consequences of LPAR2 deletion or antagonism on various aspects of cognition using a set of behavioral and electrophysiological analyses. Hippocampal neuronal network activity was decreased in middle-aged LPAR2
Identifiants
pubmed: 32468095
doi: 10.1007/s00018-020-03553-4
pii: 10.1007/s00018-020-03553-4
pmc: PMC7897625
doi:
Substances chimiques
Calcium-Binding Proteins
0
EGF Family of Proteins
0
Egfl7 protein, mouse
0
Receptors, Lysophosphatidic Acid
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1029-1050Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : CRC1039 A03
Organisme : Deutsche Forschungsgemeinschaft
ID : CRC1080 A03
Organisme : Deutsche Forschungsgemeinschaft
ID : CRC1080 B05
Organisme : Deutsche Forschungsgemeinschaft
ID : SFB1193 A05
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