The involvement of the GPR39-Zn(2+)-sensing receptor in the pathophysiology of depression. Studies in rodent models and suicide victims

Zinc is one of the most important trace elements in our body. Patients suffering from depression show lower serum zinc levels compared to healthy controls. Zincs antagonism to the glutamatergic system seems to be responsible for mood recovery. Recent years have shown that zinc may regulate neurotran...

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Published in:	Neuropharmacology Vol. 79; pp. 290 - 297
Main Authors:	Młyniec, Katarzyna, Doboszewska, Urszula, Szewczyk, Bernadeta, Sowa-Kućma, Magdalena, Misztak, Paulina, Piekoszewski, Wojciech, Trela, Franciszek, Ostachowicz, Beata, Nowak, Gabriel
Format:	Journal Article
Language:	English
Published:	England Elsevier Ltd 01.04.2014
Subjects:	Adult Animals BDNF Brain-Derived Neurotrophic Factor - metabolism CREB Cyclic AMP Response Element-Binding Protein - metabolism Depression Depressive Disorder - metabolism Disease Models, Animal Female Frontal Lobe - metabolism GPR39 Hippocampus - metabolism Humans Male Mice Mice, Inbred Strains Olfactory Bulb - physiopathology Olfactory Bulb - surgery Rats Rats, Sprague-Dawley Receptor, trkB - metabolism Receptors, G-Protein-Coupled - metabolism Signal Transduction Suicide TrkB Zinc - deficiency Zn(2+)-sensing receptor GPR39 Zn(2+)-sensing receptor Depression TrkB CREB BDNF
ISSN:	0028-3908, 1873-7064, 1873-7064
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Abstract	Zinc is one of the most important trace elements in our body. Patients suffering from depression show lower serum zinc levels compared to healthy controls. Zincs antagonism to the glutamatergic system seems to be responsible for mood recovery. Recent years have shown that zinc may regulate neurotransmission via the metabotropic GPR39 receptor. Activation of the GPR39-Zn(2+)-sensing receptor (GPR39) triggers diverse neuronal pathways leading to a cAMP-responsive element binding the protein (CREB) expression, which then induces synthesis of the brain-derived neurotrophic factor and, in turn, activation of the Tropomyosin receptor kinase B (TrkB) receptor. In the present study, we investigated the alteration of the GPR39 in different models of depression, such as zinc deficiency and olfactory bulbectomy and in suicide victims. Additionaly, we focused on CREB-BDNF/TrkB under zinc deficient conditions in mice. To demonstrate depressive-like behaviour, a standard and modified forced swim test (FST) was performed. To evaluate expression of GPR39, CREB, BDNF and TrkB, Western Blot analysis was used. Zinc deficient mice and rats showed decreased GPR39 expression in the hippocampus and frontal cortex. A decreased level of hippocampal and cortical GPR39 was also observed in suicide victims. In contrast, increased GPR39 in the hippocampus of olfactory bulbectomized rats was observed. Additionally, we found a decreased expression of CREB, BDNF and TrkB only in the hippocampus of zinc-deficient mice. Our present study demonstrates the associacion of the GPR39 Zn(2+)-sensing receptor in the pathomechanism of depression. Down-regulation of CREB, BDNF, TrkB and GPR39 receptor found under zinc-deficient conditions in the hippocampus, may play an important role in the pathophysiology of mood disorders, since most of patients suffering from depression show lower serum zinc. •Zinc deficiency causes depression-like behaviour in the modified forced swim test.•Zinc deficiency in rodents as well as suicide victims decrease the expression of the GPR39 receptor.•Zinc deficiency induces a reduction in CREB-BDNF/TrkB in the hippocampus, but not in the frontal cortex.•GPR39-down regulation may be involved in the pathophysiology of depression.
AbstractList	Zinc is one of the most important trace elements in our body. Patients suffering from depression show lower serum zinc levels compared to healthy controls. Zincs antagonism to the glutamatergic system seems to be responsible for mood recovery. Recent years have shown that zinc may regulate neurotransmission via the metabotropic GPR39 receptor. Activation of the GPR39-Zn(2+)-sensing receptor (GPR39) triggers diverse neuronal pathways leading to a cAMP-responsive element binding the protein (CREB) expression, which then induces synthesis of the brain-derived neurotrophic factor and, in turn, activation of the Tropomyosin receptor kinase B (TrkB) receptor. In the present study, we investigated the alteration of the GPR39 in different models of depression, such as zinc deficiency and olfactory bulbectomy and in suicide victims. Additionaly, we focused on CREB-BDNF/TrkB under zinc deficient conditions in mice. To demonstrate depressive-like behaviour, a standard and modified forced swim test (FST) was performed. To evaluate expression of GPR39, CREB, BDNF and TrkB, Western Blot analysis was used. Zinc deficient mice and rats showed decreased GPR39 expression in the hippocampus and frontal cortex. A decreased level of hippocampal and cortical GPR39 was also observed in suicide victims. In contrast, increased GPR39 in the hippocampus of olfactory bulbectomized rats was observed. Additionally, we found a decreased expression of CREB, BDNF and TrkB only in the hippocampus of zinc-deficient mice. Our present study demonstrates the associacion of the GPR39 Zn(2+)-sensing receptor in the pathomechanism of depression. Down-regulation of CREB, BDNF, TrkB and GPR39 receptor found under zinc-deficient conditions in the hippocampus, may play an important role in the pathophysiology of mood disorders, since most of patients suffering from depression show lower serum zinc. Zinc is one of the most important trace elements in our body. Patients suffering from depression show lower serum zinc levels compared to healthy controls. Zincs antagonism to the glutamatergic system seems to be responsible for mood recovery. Recent years have shown that zinc may regulate neurotransmission via the metabotropic GPR39 receptor. Activation of the GPR39-Zn(2+)-sensing receptor (GPR39) triggers diverse neuronal pathways leading to a cAMP-responsive element binding the protein (CREB) expression, which then induces synthesis of the brain-derived neurotrophic factor and, in turn, activation of the Tropomyosin receptor kinase B (TrkB) receptor. In the present study, we investigated the alteration of the GPR39 in different models of depression, such as zinc deficiency and olfactory bulbectomy and in suicide victims. Additionaly, we focused on CREB-BDNF/TrkB under zinc deficient conditions in mice. To demonstrate depressive-like behaviour, a standard and modified forced swim test (FST) was performed. To evaluate expression of GPR39, CREB, BDNF and TrkB, Western Blot analysis was used. Zinc deficient mice and rats showed decreased GPR39 expression in the hippocampus and frontal cortex. A decreased level of hippocampal and cortical GPR39 was also observed in suicide victims. In contrast, increased GPR39 in the hippocampus of olfactory bulbectomized rats was observed. Additionally, we found a decreased expression of CREB, BDNF and TrkB only in the hippocampus of zinc-deficient mice. Our present study demonstrates the associacion of the GPR39 Zn(2+)-sensing receptor in the pathomechanism of depression. Down-regulation of CREB, BDNF, TrkB and GPR39 receptor found under zinc-deficient conditions in the hippocampus, may play an important role in the pathophysiology of mood disorders, since most of patients suffering from depression show lower serum zinc.Zinc is one of the most important trace elements in our body. Patients suffering from depression show lower serum zinc levels compared to healthy controls. Zincs antagonism to the glutamatergic system seems to be responsible for mood recovery. Recent years have shown that zinc may regulate neurotransmission via the metabotropic GPR39 receptor. Activation of the GPR39-Zn(2+)-sensing receptor (GPR39) triggers diverse neuronal pathways leading to a cAMP-responsive element binding the protein (CREB) expression, which then induces synthesis of the brain-derived neurotrophic factor and, in turn, activation of the Tropomyosin receptor kinase B (TrkB) receptor. In the present study, we investigated the alteration of the GPR39 in different models of depression, such as zinc deficiency and olfactory bulbectomy and in suicide victims. Additionaly, we focused on CREB-BDNF/TrkB under zinc deficient conditions in mice. To demonstrate depressive-like behaviour, a standard and modified forced swim test (FST) was performed. To evaluate expression of GPR39, CREB, BDNF and TrkB, Western Blot analysis was used. Zinc deficient mice and rats showed decreased GPR39 expression in the hippocampus and frontal cortex. A decreased level of hippocampal and cortical GPR39 was also observed in suicide victims. In contrast, increased GPR39 in the hippocampus of olfactory bulbectomized rats was observed. Additionally, we found a decreased expression of CREB, BDNF and TrkB only in the hippocampus of zinc-deficient mice. Our present study demonstrates the associacion of the GPR39 Zn(2+)-sensing receptor in the pathomechanism of depression. Down-regulation of CREB, BDNF, TrkB and GPR39 receptor found under zinc-deficient conditions in the hippocampus, may play an important role in the pathophysiology of mood disorders, since most of patients suffering from depression show lower serum zinc. Zinc is one of the most important trace elements in our body. Patients suffering from depression show lower serum zinc levels compared to healthy controls. Zincs antagonism to the glutamatergic system seems to be responsible for mood recovery. Recent years have shown that zinc may regulate neurotransmission via the metabotropic GPR39 receptor. Activation of the GPR39-Zn(2+)-sensing receptor (GPR39) triggers diverse neuronal pathways leading to a cAMP-responsive element binding the protein (CREB) expression, which then induces synthesis of the brain-derived neurotrophic factor and, in turn, activation of the Tropomyosin receptor kinase B (TrkB) receptor. In the present study, we investigated the alteration of the GPR39 in different models of depression, such as zinc deficiency and olfactory bulbectomy and in suicide victims. Additionaly, we focused on CREB-BDNF/TrkB under zinc deficient conditions in mice. To demonstrate depressive-like behaviour, a standard and modified forced swim test (FST) was performed. To evaluate expression of GPR39, CREB, BDNF and TrkB, Western Blot analysis was used. Zinc deficient mice and rats showed decreased GPR39 expression in the hippocampus and frontal cortex. A decreased level of hippocampal and cortical GPR39 was also observed in suicide victims. In contrast, increased GPR39 in the hippocampus of olfactory bulbectomized rats was observed. Additionally, we found a decreased expression of CREB, BDNF and TrkB only in the hippocampus of zinc-deficient mice. Our present study demonstrates the associacion of the GPR39 Zn(2+)-sensing receptor in the pathomechanism of depression. Down-regulation of CREB, BDNF, TrkB and GPR39 receptor found under zinc-deficient conditions in the hippocampus, may play an important role in the pathophysiology of mood disorders, since most of patients suffering from depression show lower serum zinc. •Zinc deficiency causes depression-like behaviour in the modified forced swim test.•Zinc deficiency in rodents as well as suicide victims decrease the expression of the GPR39 receptor.•Zinc deficiency induces a reduction in CREB-BDNF/TrkB in the hippocampus, but not in the frontal cortex.•GPR39-down regulation may be involved in the pathophysiology of depression.
Author	Szewczyk, Bernadeta Młyniec, Katarzyna Piekoszewski, Wojciech Nowak, Gabriel Sowa-Kućma, Magdalena Misztak, Paulina Ostachowicz, Beata Doboszewska, Urszula Trela, Franciszek
Author_xml	– sequence: 1 givenname: Katarzyna surname: Młyniec fullname: Młyniec, Katarzyna email: katarzyna.mlyniec@uj.edu.pl organization: Department of Toxicology, Jagiellonian University Medical College, Medyczna 9, PL 30-688 Kraków, Poland – sequence: 2 givenname: Urszula surname: Doboszewska fullname: Doboszewska, Urszula organization: Department of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, PL 30-688 Kraków, Poland – sequence: 3 givenname: Bernadeta surname: Szewczyk fullname: Szewczyk, Bernadeta organization: Institute of Pharmacology, Polish Academy of Sciences and Center of Excellence in Neuropsychopharmacology, Smętna 12, PL 31-343 Kraków, Poland – sequence: 4 givenname: Magdalena surname: Sowa-Kućma fullname: Sowa-Kućma, Magdalena organization: Institute of Pharmacology, Polish Academy of Sciences and Center of Excellence in Neuropsychopharmacology, Smętna 12, PL 31-343 Kraków, Poland – sequence: 5 givenname: Paulina surname: Misztak fullname: Misztak, Paulina organization: Institute of Pharmacology, Polish Academy of Sciences and Center of Excellence in Neuropsychopharmacology, Smętna 12, PL 31-343 Kraków, Poland – sequence: 6 givenname: Wojciech surname: Piekoszewski fullname: Piekoszewski, Wojciech organization: Department of Analytical Chemistry Faculty of Chemistry, Jagiellonian University, Krakow, Poland – sequence: 7 givenname: Franciszek surname: Trela fullname: Trela, Franciszek organization: Department of Forensic Medicine, Jagiellonian University Medical College, Kraków, Poland – sequence: 8 givenname: Beata surname: Ostachowicz fullname: Ostachowicz, Beata organization: Faculty of Physics and Applied Computer Science, AGH University of Science and Technology, Kraków, Poland – sequence: 9 givenname: Gabriel surname: Nowak fullname: Nowak, Gabriel organization: Department of Pharmacobiology, Jagiellonian University Medical College, Medyczna 9, PL 30-688 Kraków, Poland
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/24333148$$D View this record in MEDLINE/PubMed
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Snippet	Zinc is one of the most important trace elements in our body. Patients suffering from depression show lower serum zinc levels compared to healthy controls....
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SubjectTerms	Adult Animals BDNF Brain-Derived Neurotrophic Factor - metabolism CREB Cyclic AMP Response Element-Binding Protein - metabolism Depression Depressive Disorder - metabolism Disease Models, Animal Female Frontal Lobe - metabolism GPR39 Hippocampus - metabolism Humans Male Mice Mice, Inbred Strains Olfactory Bulb - physiopathology Olfactory Bulb - surgery Rats Rats, Sprague-Dawley Receptor, trkB - metabolism Receptors, G-Protein-Coupled - metabolism Signal Transduction Suicide TrkB Zinc - deficiency Zn(2+)-sensing receptor
Title	The involvement of the GPR39-Zn(2+)-sensing receptor in the pathophysiology of depression. Studies in rodent models and suicide victims
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