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

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Glucose-dependent insulinotropic polypeptide receptor knockout mice are impaired in learning, synaptic plasticity, and neurogenesis. / Faivre, Emilie; Gault, Victor A.; Thorens, Bernard; Hölscher, Christian.

In: Journal of Neurophysiology, Vol. 105, No. 4, 01.04.2011, p. 1574-1580.

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Faivre, Emilie ; Gault, Victor A. ; Thorens, Bernard ; Hölscher, Christian. / Glucose-dependent insulinotropic polypeptide receptor knockout mice are impaired in learning, synaptic plasticity, and neurogenesis. In: Journal of Neurophysiology. 2011 ; Vol. 105, No. 4. pp. 1574-1580.

Bibtex

@article{484fddb5b3a8477d9b749f1eaf8a1b27,
title = "Glucose-dependent insulinotropic polypeptide receptor knockout mice are impaired in learning, synaptic plasticity, and neurogenesis",
abstract = "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.",
keywords = "Animals, Cell Proliferation, Cognition, Learning, Locomotion, Long-Term Potentiation, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Models, Animal, Neurogenesis, Neuronal Plasticity, Receptors, Gastrointestinal Hormone, Synapses, Synaptic Transmission",
author = "Emilie Faivre and Gault, {Victor A.} and Bernard Thorens and Christian H{\"o}lscher",
year = "2011",
month = apr
day = "1",
doi = "10.1152/jn.00866.2010",
language = "English",
volume = "105",
pages = "1574--1580",
journal = "Journal of Neurophysiology",
issn = "0022-3077",
publisher = "American Physiological Society",
number = "4",

}

RIS

TY - JOUR

T1 - Glucose-dependent insulinotropic polypeptide receptor knockout mice are impaired in learning, synaptic plasticity, and neurogenesis

AU - Faivre, Emilie

AU - Gault, Victor A.

AU - Thorens, Bernard

AU - Hölscher, Christian

PY - 2011/4/1

Y1 - 2011/4/1

N2 - 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.

AB - 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.

KW - Animals

KW - Cell Proliferation

KW - Cognition

KW - Learning

KW - Locomotion

KW - Long-Term Potentiation

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Models, Animal

KW - Neurogenesis

KW - Neuronal Plasticity

KW - Receptors, Gastrointestinal Hormone

KW - Synapses

KW - Synaptic Transmission

U2 - 10.1152/jn.00866.2010

DO - 10.1152/jn.00866.2010

M3 - Journal article

C2 - 21273318

VL - 105

SP - 1574

EP - 1580

JO - Journal of Neurophysiology

JF - Journal of Neurophysiology

SN - 0022-3077

IS - 4

ER -