GPR39 (Zinc Receptor) Knockout Mice Exhibit Depression-Like Behavior and CREB/BDNF Down-Regulation in the Hippocampus

Background:Zinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors.Methods:In the present study, we investigated whether GPR39 knockout would cause depressive-like and/or anxiety-like behavior, as measured by the forced swim test, tail suspe...

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Published in:	The international journal of neuropsychopharmacology Vol. 18; no. 3; pp. 1 - 8
Main Authors:	Młyniec, Katarzyna, Budziszewska, Bogusława, Holst, Birgitte, Ostachowicz, Beata, Nowak, Gabriel
Format:	Journal Article
Language:	English
Published:	US Oxford University Press 01.02.2015
Subjects:	Animals Anxiety Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - metabolism Corticosterone - blood CREB-Binding Protein - metabolism Dark Adaptation - genetics Depression - genetics Depression - metabolism Depression - pathology Disease Models, Animal Down-Regulation - genetics Hindlimb Suspension Hippocampus - metabolism Hypothalamus Immobility Response, Tonic - physiology Kinases Male Mental depression Mice Mice, Inbred C57BL Mice, Knockout Motor Activity - genetics Proteins Receptor, trkB - metabolism Receptors, G-Protein-Coupled - deficiency Receptors, G-Protein-Coupled - genetics Swimming - psychology Time Factors Zinc - metabolism GPR39 HPA axis CREB depression zinc receptor
ISSN:	1461-1457, 1469-5111, 1469-5111
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Abstract	Background:Zinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors.Methods:In the present study, we investigated whether GPR39 knockout would cause depressive-like and/or anxiety-like behavior, as measured by the forced swim test, tail suspension test, and light/dark test. We also investigated whether lack of GPR39 would change levels of cAMP response element-binding protein (CREB),brain-derived neurotrophic factor (BDNF) and tropomyosin related kinase B (TrkB) protein in the hippocampus and frontal cortex of GPR39 knockout mice subjected to the forced swim test, as measured by Western-blot analysis.Results:In this study, GPR39 knockout mice showed an increased immobility time in both the forced swim test and tail suspension test, indicating depressive-like behavior and displayed anxiety-like phenotype. GPR39 knockout mice had lower CREB and BDNF levels in the hippocampus, but not in the frontal cortex, which indicates region specificity for the impaired CREB/BDNF pathway (which is important in antidepressant response) in the absence of GPR39. There were no changes in TrkB protein in either structure. In the present study, we also investigated activity in the hypothalamus-pituitary-adrenal axis under both zinc- and GPR39-deficient conditions. Zinc-deficient mice had higher serum corticosterone levels and lower glucocorticoid receptor levels in the hippocampus and frontal cortex.Conclusions:There were no changes in the GPR39 knockout mice in comparison with the wild-type control mice, which does not support a role of GPR39 in hypothalamus-pituitary-adrenal axis regulation. The results of this study indicate the involvement of the GPR39 Zn2+-sensing receptor in the pathophysiology of depression with component of anxiety.
AbstractList	Zinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors. In the present study, we investigated whether GPR39 knockout would cause depressive-like and/or anxiety-like behavior, as measured by the forced swim test, tail suspension test, and light/dark test. We also investigated whether lack of GPR39 would change levels of cAMP response element-binding protein (CREB),brain-derived neurotrophic factor (BDNF) and tropomyosin related kinase B (TrkB) protein in the hippocampus and frontal cortex of GPR39 knockout mice subjected to the forced swim test, as measured by Western-blot analysis. In this study, GPR39 knockout mice showed an increased immobility time in both the forced swim test and tail suspension test, indicating depressive-like behavior and displayed anxiety-like phenotype. GPR39 knockout mice had lower CREB and BDNF levels in the hippocampus, but not in the frontal cortex, which indicates region specificity for the impaired CREB/BDNF pathway (which is important in antidepressant response) in the absence of GPR39. There were no changes in TrkB protein in either structure. In the present study, we also investigated activity in the hypothalamus-pituitary-adrenal axis under both zinc- and GPR39-deficient conditions. Zinc-deficient mice had higher serum corticosterone levels and lower glucocorticoid receptor levels in the hippocampus and frontal cortex. There were no changes in the GPR39 knockout mice in comparison with the wild-type control mice, which does not support a role of GPR39 in hypothalamus-pituitary-adrenal axis regulation. The results of this study indicate the involvement of the GPR39 Zn(2+)-sensing receptor in the pathophysiology of depression with component of anxiety. Background:Zinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors.Methods:In the present study, we investigated whether GPR39 knockout would cause depressive-like and/or anxiety-like behavior, as measured by the forced swim test, tail suspension test, and light/dark test. We also investigated whether lack of GPR39 would change levels of cAMP response element-binding protein (CREB),brain-derived neurotrophic factor (BDNF) and tropomyosin related kinase B (TrkB) protein in the hippocampus and frontal cortex of GPR39 knockout mice subjected to the forced swim test, as measured by Western-blot analysis.Results:In this study, GPR39 knockout mice showed an increased immobility time in both the forced swim test and tail suspension test, indicating depressive-like behavior and displayed anxiety-like phenotype. GPR39 knockout mice had lower CREB and BDNF levels in the hippocampus, but not in the frontal cortex, which indicates region specificity for the impaired CREB/BDNF pathway (which is important in antidepressant response) in the absence of GPR39. There were no changes in TrkB protein in either structure. In the present study, we also investigated activity in the hypothalamus-pituitary-adrenal axis under both zinc- and GPR39-deficient conditions. Zinc-deficient mice had higher serum corticosterone levels and lower glucocorticoid receptor levels in the hippocampus and frontal cortex.Conclusions:There were no changes in the GPR39 knockout mice in comparison with the wild-type control mice, which does not support a role of GPR39 in hypothalamus-pituitary-adrenal axis regulation. The results of this study indicate the involvement of the GPR39 Zn2+-sensing receptor in the pathophysiology of depression with component of anxiety. Background: Zinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors. Methods: In the present study, we investigated whether GPR39 knockout would cause depressive-like and/or anxiety-like behavior, as measured by the forced swim test, tail suspension test, and light/dark test. We also investigated whether lack of GPR39 would change levels of cAMP response element-binding protein (CREB), brain-derived neurotrophic factor (BDNF) and tropomyosin related kinase B (TrkB) protein in the hippocampus and frontal cortex of GPR39 knockout mice subjected to the forced swim test, as measured by Western-blot analysis. Results: In this study, GPR39 knockout mice showed an increased immobility time in both the forced swim test and tail suspension test, indicating depressive-like behavior and displayed anxiety-like phenotype. GPR39 knockout mice had lower CREB and BDNF levels in the hippocampus, but not in the frontal cortex, which indicates region specificity for the impaired CREB/BDNF pathway (which is important in antidepressant response) in the absence of GPR39. There were no changes in TrkB protein in either structure. In the present study, we also investigated activity in the hypothalamus-pituitary-adrenal axis under both zinc- and GPR39-deficient conditions. Zinc-deficient mice had higher serum corticosterone levels and lower glucocorticoid receptor levels in the hippocampus and frontal cortex. Conclusions: There were no changes in the GPR39 knockout mice in comparison with the wild-type control mice, which does not support a role of GPR39 in hypothalamus-pituitary-adrenal axis regulation. The results of this study indicate the involvement of the GPR39 Zn super(2+)-sensing receptor in the pathophysiology of depression with component of anxiety. Zinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors.BACKGROUNDZinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors.In the present study, we investigated whether GPR39 knockout would cause depressive-like and/or anxiety-like behavior, as measured by the forced swim test, tail suspension test, and light/dark test. We also investigated whether lack of GPR39 would change levels of cAMP response element-binding protein (CREB),brain-derived neurotrophic factor (BDNF) and tropomyosin related kinase B (TrkB) protein in the hippocampus and frontal cortex of GPR39 knockout mice subjected to the forced swim test, as measured by Western-blot analysis.METHODSIn the present study, we investigated whether GPR39 knockout would cause depressive-like and/or anxiety-like behavior, as measured by the forced swim test, tail suspension test, and light/dark test. We also investigated whether lack of GPR39 would change levels of cAMP response element-binding protein (CREB),brain-derived neurotrophic factor (BDNF) and tropomyosin related kinase B (TrkB) protein in the hippocampus and frontal cortex of GPR39 knockout mice subjected to the forced swim test, as measured by Western-blot analysis.In this study, GPR39 knockout mice showed an increased immobility time in both the forced swim test and tail suspension test, indicating depressive-like behavior and displayed anxiety-like phenotype. GPR39 knockout mice had lower CREB and BDNF levels in the hippocampus, but not in the frontal cortex, which indicates region specificity for the impaired CREB/BDNF pathway (which is important in antidepressant response) in the absence of GPR39. There were no changes in TrkB protein in either structure. In the present study, we also investigated activity in the hypothalamus-pituitary-adrenal axis under both zinc- and GPR39-deficient conditions. Zinc-deficient mice had higher serum corticosterone levels and lower glucocorticoid receptor levels in the hippocampus and frontal cortex.RESULTSIn this study, GPR39 knockout mice showed an increased immobility time in both the forced swim test and tail suspension test, indicating depressive-like behavior and displayed anxiety-like phenotype. GPR39 knockout mice had lower CREB and BDNF levels in the hippocampus, but not in the frontal cortex, which indicates region specificity for the impaired CREB/BDNF pathway (which is important in antidepressant response) in the absence of GPR39. There were no changes in TrkB protein in either structure. In the present study, we also investigated activity in the hypothalamus-pituitary-adrenal axis under both zinc- and GPR39-deficient conditions. Zinc-deficient mice had higher serum corticosterone levels and lower glucocorticoid receptor levels in the hippocampus and frontal cortex.There were no changes in the GPR39 knockout mice in comparison with the wild-type control mice, which does not support a role of GPR39 in hypothalamus-pituitary-adrenal axis regulation. The results of this study indicate the involvement of the GPR39 Zn(2+)-sensing receptor in the pathophysiology of depression with component of anxiety.CONCLUSIONSThere were no changes in the GPR39 knockout mice in comparison with the wild-type control mice, which does not support a role of GPR39 in hypothalamus-pituitary-adrenal axis regulation. The results of this study indicate the involvement of the GPR39 Zn(2+)-sensing receptor in the pathophysiology of depression with component of anxiety.
Author	Holst, Birgitte Młyniec, Katarzyna Ostachowicz, Beata Budziszewska, Bogusława Nowak, Gabriel
Author_xml	– sequence: 1 givenname: Katarzyna surname: Młyniec fullname: Młyniec, Katarzyna organization: Department of Biochemical Toxicology, Jagiellonian University Medical College, Medyczna 9, PL 30–688 Kraków, Poland (Dr. K. Młyniec, Prof. B. Budziszewska); Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, PL 31–343 Kraków, Poland (Profs. B. Budziszewska, G. Nowak); Department of Neuroscience and Pharmacology University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen, Denmark (Prof. B. Holst); Faculty of Physics and Applied Computer Science, AGH University of Science and Technology, Kraków, Poland (Dr. B. Ostachowicz); Department of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, PL 30–688 Kraków, Poland (Prof. G. Nowak) – sequence: 2 givenname: Bogusława surname: Budziszewska fullname: Budziszewska, Bogusława organization: Department of Biochemical Toxicology, Jagiellonian University Medical College, Medyczna 9, PL 30–688 Kraków, Poland (Dr. K. Młyniec, Prof. B. Budziszewska); Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, PL 31–343 Kraków, Poland (Profs. B. Budziszewska, G. Nowak); Department of Neuroscience and Pharmacology University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen, Denmark (Prof. B. Holst); Faculty of Physics and Applied Computer Science, AGH University of Science and Technology, Kraków, Poland (Dr. B. Ostachowicz); Department of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, PL 30–688 Kraków, Poland (Prof. G. Nowak) – sequence: 3 givenname: Birgitte surname: Holst fullname: Holst, Birgitte organization: Department of Biochemical Toxicology, Jagiellonian University Medical College, Medyczna 9, PL 30–688 Kraków, Poland (Dr. K. Młyniec, Prof. B. Budziszewska); Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, PL 31–343 Kraków, Poland (Profs. B. Budziszewska, G. Nowak); Department of Neuroscience and Pharmacology University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen, Denmark (Prof. B. Holst); Faculty of Physics and Applied Computer Science, AGH University of Science and Technology, Kraków, Poland (Dr. B. Ostachowicz); Department of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, PL 30–688 Kraków, Poland (Prof. G. Nowak) – sequence: 4 givenname: Beata surname: Ostachowicz fullname: Ostachowicz, Beata organization: Department of Biochemical Toxicology, Jagiellonian University Medical College, Medyczna 9, PL 30–688 Kraków, Poland (Dr. K. Młyniec, Prof. B. Budziszewska); Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, PL 31–343 Kraków, Poland (Profs. B. Budziszewska, G. Nowak); Department of Neuroscience and Pharmacology University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen, Denmark (Prof. B. Holst); Faculty of Physics and Applied Computer Science, AGH University of Science and Technology, Kraków, Poland (Dr. B. Ostachowicz); Department of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, PL 30–688 Kraków, Poland (Prof. G. Nowak) – sequence: 5 givenname: Gabriel surname: Nowak fullname: Nowak, Gabriel organization: Department of Biochemical Toxicology, Jagiellonian University Medical College, Medyczna 9, PL 30–688 Kraków, Poland (Dr. K. Młyniec, Prof. B. Budziszewska); Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, PL 31–343 Kraków, Poland (Profs. B. Budziszewska, G. Nowak); Department of Neuroscience and Pharmacology University of Copenhagen, Blegdamsvej 3, DK-2200, Copenhagen, Denmark (Prof. B. Holst); Faculty of Physics and Applied Computer Science, AGH University of Science and Technology, Kraków, Poland (Dr. B. Ostachowicz); Department of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, PL 30–688 Kraków, Poland (Prof. G. Nowak)
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Keywords	GPR39 HPA axis CREB depression zinc receptor
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PublicationDateYYYYMMDD	2015-02-01
PublicationDate_xml	– month: 02 year: 2015 text: 2015-02-01 day: 01
PublicationDecade	2010
PublicationPlace	US
PublicationPlace_xml	– name: US – name: England – name: Oxford
PublicationTitle	The international journal of neuropsychopharmacology
PublicationTitleAlternate	Int J Neuropsychopharmacol
PublicationYear	2015
Publisher	Oxford University Press
Publisher_xml	– name: Oxford University Press
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Snippet	Background:Zinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors.Methods:In the present study, we... Zinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors. In the present study, we investigated... Zinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors.BACKGROUNDZinc may act as a neurotransmitter... Background: Zinc may act as a neurotransmitter in the central nervous system by activation of the GPR39 metabotropic receptors. Methods: In the present study,...
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SubjectTerms	Animals Anxiety Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - metabolism Corticosterone - blood CREB-Binding Protein - metabolism Dark Adaptation - genetics Depression - genetics Depression - metabolism Depression - pathology Disease Models, Animal Down-Regulation - genetics Hindlimb Suspension Hippocampus - metabolism Hypothalamus Immobility Response, Tonic - physiology Kinases Male Mental depression Mice Mice, Inbred C57BL Mice, Knockout Motor Activity - genetics Proteins Receptor, trkB - metabolism Receptors, G-Protein-Coupled - deficiency Receptors, G-Protein-Coupled - genetics Swimming - psychology Time Factors Zinc - metabolism
Title	GPR39 (Zinc Receptor) Knockout Mice Exhibit Depression-Like Behavior and CREB/BDNF Down-Regulation in the Hippocampus
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