Investigation of the GPR39 zinc receptor following inhibition of monoaminergic neurotransmission and potentialization of glutamatergic neurotransmission

Młyniec, Katarzyna; Gaweł, Magdalena; Librowski, Tadeusz; Reczyński, Witold; Bystrowska, Beata; Holst, Birgitte

doi:10.1016/j.brainresbull.2015.04.005

Cited by 29 publications

(25 citation statements)

References 43 publications

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“…A 10-day administration of pCPA, an inhibitor of 5-HT synthesis, caused downregulation of GPR39 protein in the hippocampus of mice [55], which suggests a link between GPR39 and 5-HT signaling. There was also a decrease in the level of 5-HT precursor, tryptophan, in the hippocampus of GPR39 knockout mice [55].…”

Section: Serotonin (5-ht)mentioning

confidence: 99%

“…There was also a decrease in the level of 5-HT precursor, tryptophan, in the hippocampus of GPR39 knockout mice [55]. Moreover, there is some evidence indicating a link between GPR39 and 5-HT 1A receptors function.…”

Section: Serotonin (5-ht)mentioning

confidence: 99%

“…While imipramine and reboxetine reduced immobility time in the FST in wild-type (WT) mice, they were inactive in this test in GPR39 knockout mice, suggesting that the GPR39 receptor is required for the antidepressant effect of antidepressants targeting the noradrenergic system [71]. Moreover, administration of α -methyl-p-tyrosine, an inhibitor of tyrosine hydroxylase, the rate-limiting enzyme in NE synthesis, which causes inhibition of NE and DA synthesis, induced upregulation of the GPR39 protein level in the frontal cortex after a 3-day administration and downregulation of this receptor in the hippocampus after a 10-day administration [55], indicating a possible role of the GPR39 receptor in NE transmission.…”

Section: Norepinephrine (Ne)mentioning

confidence: 99%

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Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity

et al. 2017

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Preclinical and clinical studies have demonstrated that zinc possesses antidepressant properties and that it may augment the therapy with conventional, that is, monoamine-based, antidepressants. In this review we aim to discuss the role of zinc in the pathophysiology and treatment of depression with regard to the monoamine hypothesis of the disease. Particular attention will be paid to the recently described zinc-sensing GPR39 receptor as well as aspects of zinc deficiency. Furthermore, an attempt will be made to give a possible explanation of the mechanisms by which zinc interacts with the monoamine system in the context of depression and neural plasticity.

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Section: Serotonin (5-ht)mentioning

confidence: 99%

Section: Serotonin (5-ht)mentioning

confidence: 99%

Section: Norepinephrine (Ne)mentioning

confidence: 99%

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Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity

et al. 2017

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“…During synaptic activity, zinc is released and serves as signal ion. Enriched in the synaptic cleft, zinc can modulate synaptic signal transduction via the modulation of glutamate receptors, ion channels, cell adhesion molecules, and the pre-or postsynaptic uptake of calcium [82] or may directly act as neurotransmitter via metabotropic GPR39 receptor (GPR39) [108] that is involved in glutamatergic transmission [109]. For example, zinc can allosterically inhibit NMDA receptors through binding to a subunit at low levels or inhibit NMDAR in a voltagedependent manner at high levels [110] and therefore modulate the signal transduction at the postsynaptic site.…”

Section: Zinc and The Brainmentioning

confidence: 99%

“…Given the multifaceted action of zinc in the brain (Figure 3), it is not surprising that zinc deficiency leads to alterations in cognitive performance and behavior in animal models and possibly humans. Acute zinc-deficient animals demonstrated impaired learning and memory behavior [119][120][121][122], increased aggressiveness [123] and hyperreactivity/irritability [98], and anxiety as well as depressive-like behavior [109,124]. Additionally, neurosensory functions like smell and taste are impaired through zinc deficiency [125].…”

Section: Zinc and The Brainmentioning

confidence: 99%

Zinc Deficiency

Sauer¹,

Hagmeyer²,

Grabrucker³

2016

Nutritional Deficiency

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Zinc is an essential trace element for humans and plays a critical role both as a structural component of proteins and as a cofactor in about 300 enzymes. Zinc deficiency was, for example, reported to affect the immune response and the endocrine system and to induce and modify brain disorders. Besides hereditary zinc deficiency, zinc deficiency-at least in mild forms-is nowadays a very abundant health issue. Today, an estimated 20% of the population worldwide is at risk of developing zinc deficiency with a high number also in industrialized countries. The major risk factors to develop zinc deficiency in industrialized nations are aging and pregnancy. Mechanistic and behavioral studies on the effects of zinc deficiency have mainly been performed using animal models. However, in combination with the few studies on human subjects, a picture emerges that shows importance of adequate nutritional zinc supply for many processes in the body. Especially the immune system and brain development and function seem to be highly sensitive to zinc deficiency. Here, we provide an overview on the effects of zinc deficiency on different organ systems, biological processes, and the associations of zinc deficiency with pathologies observed in humans and animal models.

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Neuro-psychopharmacological perspective of Orphan receptors of Rhodopsin (class A) family of G protein-coupled receptors

Khan

2017

Psychopharmacology

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This review presents a neuropsychopharmacological perspective of 26 orphan receptors of rhodopsin (class A) family, namely GPR3, GPR6, GPR12, GPR17, GPR26, GPR35, GPR39, GPR48, GPR49, GPR50, GPR52, GPR55, GPR61, GPR62, GPR63, GPR68, GPR75, GPR78, GPR83, GPR84, GPR85, GPR88, GPR153, GPR162, GPR171, and TAAR6. We discussed the expression of these receptors in mammalian brain and their physiological roles. Furthermore, we have briefly highlighted their roles in neurodegenerative diseases and psychiatric disorders including Alzheimer's disease, Parkinson's disease, neuroinflammation, inflammatory pain, bipolar and schizophrenic disorders, epilepsy, anxiety, and depression.

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Investigation of the GPR39 zinc receptor following inhibition of monoaminergic neurotransmission and potentialization of glutamatergic neurotransmission

Cited by 29 publications

References 43 publications

Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity

Zinc in the Monoaminergic Theory of Depression: Its Relationship to Neural Plasticity

Zinc Deficiency

Neuro-psychopharmacological perspective of Orphan receptors of Rhodopsin (class A) family of G protein-coupled receptors

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