Glucose-dependent insulinotropic polypeptide receptor knockout mice are impaired in learning, synaptic plasticity, and neurogenesis.

Détails

ID Serval
serval:BIB_CBB8AAFE016B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Glucose-dependent insulinotropic polypeptide receptor knockout mice are impaired in learning, synaptic plasticity, and neurogenesis.
Périodique
Journal of Neurophysiology
Auteur(s)
Faivre E., Gault V.A., Thorens B., Hölscher C.
ISSN
1522-1598 (Electronic)
ISSN-L
0022-3077
Statut éditorial
Publié
Date de publication
2011
Volume
105
Numéro
4
Pages
1574-1580
Langue
anglais
Résumé
Glucose-dependent insulinotropic polypeptide (GIP) is a key incretin hormone, released from intestine after a meal, producing a glucose-dependent insulin secretion. The GIP receptor (GIPR) is expressed on pyramidal neurons in the cortex and hippocampus, and GIP is synthesized in a subset of neurons in the brain. However, the role of the GIPR in neuronal signaling is not clear. In this study, we used a mouse strain with GIPR gene deletion (GIPR KO) to elucidate the role of the GIPR in neuronal communication and brain function. Compared with C57BL/6 control mice, GIPR KO mice displayed higher locomotor activity in an open-field task. Impairment of recognition and spatial learning and memory of GIPR KO mice were found in the object recognition task and a spatial water maze task, respectively. In an object location task, no impairment was found. GIPR KO mice also showed impaired synaptic plasticity in paired-pulse facilitation and a block of long-term potentiation in area CA1 of the hippocampus. Moreover, a large decrease in the number of neuronal progenitor cells was found in the dentate gyrus of transgenic mice, although the numbers of young neurons was not changed. Together the results suggest that GIP receptors play an important role in cognition, neurotransmission, and cell proliferation.
Mots-clé
Animals, Cell Proliferation, Cognition/physiology, Learning/physiology, Locomotion/genetics, Locomotion/physiology, Long-Term Potentiation/genetics, Long-Term Potentiation/physiology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Models, Animal, Neurogenesis/genetics, Neurogenesis/physiology, Neuronal Plasticity/genetics, Neuronal Plasticity/physiology, Receptors, Gastrointestinal Hormone/deficiency, Receptors, Gastrointestinal Hormone/genetics, Synapses/genetics, Synapses/physiology, Synaptic Transmission/genetics, Synaptic Transmission/physiology
Pubmed
Web of science
Création de la notice
28/03/2011 10:26
Dernière modification de la notice
20/08/2019 15:46
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