Mechanism of Manganese Dysregulation of Dopamine Neuronal Activity

 produces a Ca2+ channel-mediated current, which increases neurotransmitter release and rhythmic firing activity of 

 concentration-dependently increased the excitability of 

 neurons, decreased the amplitude of action potentials, and narrowed action potential width.

[Neural differentiation of pluripotent stem cells and application for metal-induced neural toxicity study].

Pathophysiology of manganese-associated neurotoxicity.

Dr. Guilarte's experimental, non-human primate model of Mn neurotoxicity suggests that

 release in the brain without loss of neuronal integrity markers, including dopamine.

Manganese neurotoxicity and glutamate-GABA interaction

Several in vivo and in vitro studies have linked increased

 concentrations with alterations in the content and metabolism of neurotransmitters, namely 

, gamma-aminobutyric acid, and glutamate.

Role of dopamine in manganese neurotoxicity

Therefore, the decreased availability or autoxidation of

Manganese neurotoxicity: effects of varying oxygen tension and EDTA on dopamine auto-oxidation.

 was more potent than other transition metal ions at stimulating 

Serum prolactin rises in Mexican school children exposed to airborne manganese.

 as a tonic inhibitor of prolactin release in the anterior hypophysis, thus the serum prolactin levels in occupationally 

 exposed workers has been found increased.

Effect of manganese exposure on the neuroendocrine system in welders.

 suppresses the inhibitory feedback control of 

Dopamine toxicity in neuroblastoma cells: role of glutathione depletion by l-BSO and apoptosis

 (200 microM), although not cytotoxic when individually administered to SK-N-SH cells, had a synergistic action on cytotoxicity.

These results suggest that DA toxicity is tightly linked to intracellular oxidant/antioxidant levels, and that environmental factors, such as excessive

 exposure, may modulate cellular sensitivity to 

Protective effect of gamma-oryzanol against manganese-induced toxicity in Drosophila melanogaster

 levels and in tyrosine hydroxylase activity, as well as in mitochondrial and cellular viability.

Early postnatal manganese exposure causes arousal dysregulation and lasting hypofunctioning of the prefrontal cortex catecholaminergic systems

 exposure reduced the evoked release of norepinephrine (NE) and caused decreased protein levels of tyrosine hydroxylase (TH), 

 (DA) and NE transporters, and DA D1 receptors, along with increased DA D2 receptors.

Neuroprotective effects of docosahexaenoic acid against sub-acute manganese intoxication induced dopaminergic and motor disorders in mice

 neurotransmission by altering tyrosine hydroxylase activity in the nigrostriatal pathway while in pretreated animals, DHA prevented this disruption.

Manganese exposure exacerbates progressive motor deficits and neurodegeneration in the MitoPark mouse model of Parkinson's disease: Relevance to gene and environment interactions in metal neurotoxicity

 exposure intensified the depletion of striatal 

 and nigral TH neuronal loss in MitoPark mice.

Metabolic effects of manganese in the nematode Caenorhabditis elegans through DAergic pathway and transcription factors activation

DAergic neurons viability were not altered by Mn, however the

 levels were significantly reduced following 

Subchronic, Low-Level Intraperitoneal Injections of Manganese (IV) Oxide and Manganese (II) Chloride Affect Rat Brain Neurochemistry

 concentrations increased in the striatum, the rest of the brain, and in plasma, and regional brain neurotransmitter concentrations, including noradrenaline, dopamine (

), 5-hydroxytrytamine, glutamate, taurine, and γ-amino butyric acid, and the activity of acetylcholinesterase changed.

Peumus boldus (Boldo) Aqueous Extract Present Better Protective Effect than Boldine Against Manganese-Induced Toxicity in D. melanogaster

Finally, we found that flies treated with

The Role of Autophagy Dysregulation in Manganese-Induced Dopaminergic Neurodegeneration

 levels and D1 dopamine receptor expression.

Altered striatal dopamine release following a sub-acute exposure to manganese

Together, these findings indicate that repeated

 exposure has long-term effects on the regulation of exocytotic 

 in the striatum, which may be involved in the mechanism underlying manganese toxicity.

Effects of manganese on tyrosine hydroxylase (TH) activity and TH-phosphorylation in a dopaminergic neural cell line.

 exposure can affect the enzymatic activity of TH, the rate-limiting enzyme in 

 synthesis, by activating PKCδ-PP2A signaling pathway in a dopaminergic cell model.

Manganese-induced NF-kappaB activation and nitrosative stress is decreased by estrogen in juvenile mice.

 treatment caused alterations in levels of striatal 

, as well as increases in NF-κB reporter activity and NOS2 expression in both microglia and astrocytes that were prevented by supplementation with E2.

Dopaminergic system activity and cellular defense mechanisms in the striatum and striatal synaptosomes of the rat subchronically exposed to manganese

 and GSH and increased levels of DHAA and uric acid both in the striatum and synaptosomes.

Molecular mechanism of manganese exposure-induced dopaminergic toxicity

 (DA) interaction-induced cell death remains unclear, here, we showed that Mn exposure alone to mesencephalic cells for 24h induced minimal apoptotic cell death.

This was further confirmed by the cell viability assay to support our hypothesis that

 and causes cells to be more susceptible.

 markedly induced induction of NOS (iNOS) expression.

The neurotoxic effects of manganese on the dopaminergic innervation of the gill of the bivalve mollusc, Crassostrea virginica.

 levels in the cerebral and visceral ganglia, and gills, but not serotonin levels.

The interaction of manganese nanoparticles with PC-12 cells induces dopamine depletion.

These results clearly demonstrate that nanoscale

, DOPAC, and HVA in a dose-dependent manner.

Guanine nucleotides do not inhibit tritiated dopamine agonist binding to bovine striatal membranes

 both in the presence and absence of GTP, but NaCl (100 mM) had no effect.

Effect of high dietary manganese intake of neonatal rats on tissue mineral accumulation, striatal dopamine levels, and neurodevelopmental status.

Brains of animals killed on day 40 showed a significant inverse relationship between

Striatal manganese accumulation induces changes in dopamine metabolism in the cirrhotic rat

 alters dopaminergic transmission promoting an increase in the turnover of 

Striatal contents of DA in cirrhotic rats diminished by 30% (P<0.05), administration of 0.5 mg/ml of manganese in drinking water to these rats returned dopamine to the basal level and 1 mg/ml of

Enhancing Effect of Manganese on L‐DOPA‐Induced Apoptosis in PC12 Cells

 (DA) metabolism (i.e., increases in DA and its acidic metabolite levels in both cell lysate and incubation medium).

Manganese: A transition metal protects nigrostriatal neurons from oxidative stress in the iron-induced animal model of Parkinsonism

 turnover and contralateral turning behaviour induced by iron.

Cellular defence mechanisms in the striatum of young and aged rats subchronically exposed to manganese

 induced biphasic changes in the levels of 

, DOPAC, HVA (an increase at the lower dose and a decrease at the higher dose) and DHAA (opposite changes).

Central nervous system toxicity of manganese. I. Inhibition of spontaneous motor activity in rats after intrathecal administration of manganese chloride.

 results in a substantial decrease in striatal 

 but not homovanillic acid or 3,4-dihydroxyphenylacetic acid (DOPAC) concentrations and is associated with an increase in the Mn concentration of the substantia nigra and caudate-putamen.

Monoaminergic systems activity and cellular defense mechanisms in the brainstem of young and aged rats subchronically exposed to manganese

 (Mn) significantly decreased levels of NA, 

 and GSH and increased 5-HIAA/5-HT ratio values and DHAA and uric acid levels.

Indications from Mn-quenching of Fura-2 fluorescence in melanotrophs that dopamine and baclofen close Ca channels that are spontaneously open but not those opened by high [K+]O; and that Cd preferentially blocks the latter.

 quenching and so, too, did the GABAB agonist, baclofen; and these effects like those of the two agonists on secretion and [Ca2+]… were blocked by the specific D2 and GABAB antagonists, sulpiride and CGP 35348, respectively, and were lost following exposure to pertussis toxin.

Dopamine metabolism alterations in a manganese-treated pheochromocytoma cell line (PC12).

Besides eliciting a specific toxic effect on PC12 cells,

 induced the complete disappearance of extracellular (free) but not intracellular (vesicle stored) 

 and its metabolite 3,4-dihydroxyphenylacetic acid.

Rat striatal dopamine and tetrahydrobiopterin content following an intrastriatal injection of manganese chloride.

 into the rat corpus striatum causes a rapid fall in the biopterin and dopamine (

Effect of low protein diet on manganese neurotoxicity: III. Brain neurotransmitter levels.

 exposure in either diet group resulted in a significant increase in the 

 and NE levels but a decrease in the 5-HT level.

Neurotransmitters and neurotransmitter receptors in developing and adult rats during manganese poisoning.

Alterations in brain dopamine and GABA following inorganic or organic manganese administration.

 to mice in the form of MnCl2 (4%) in the diet for 6 months or injections of the organic fuel-additive methylcyclopentadienyl manganese tricarbonyl (MMT) for 3 weeks resulted in a decrease in 

 concentrations in the striatum and olfactory tubercles.

Chronic Manganese Treatment of Rats Alters Synaptosomal Uptake of Dopamine and the Behavioural Response to Amphetamine Administration

 treatment from conception onward resulted in increased striatal synaptosomal uptake of 

, but not of a variety of other neurotransmitters/precursors in 80‐day‐old rats.

The Effects of Chronic Manganese Chloride Treatment Expressed as Age‐Dependent, Transient Changes in Rat Brain Synaptosomal Uptake of Amines

 treatment of rats from conception onwards, a decrease was observed in the uptake of 

, but not of noradrenaline or serotonin, by synaptosomes isolated from hypothalamus, striatum, and midbrain and in choline uptake by hypothalamic synaptosomes obtained from 70–90‐day‐old animals.

Concentrations of Striatal Catecholamines in Rats Given Manganese Chloride Through Drinking Water

 treatment produced an initial increase in the contents of dopamine (

), norepinephrine (NE), homovanillic acid (H VA) and tyrosine in the corpus striatum.

Effect of manganese on synthesis of brain catecholamines in growing rats.

 and norepinephrine to a greater extent in the brains of treated animals.

Enhanced autoxidation of dopamine as a possible basis of manganese neurotoxicity.

, may augment considerably the production of neurotoxins emanating from this process and, under in vivo conditions, could be expected to contribute significantly to the neurodegenerative changes that accompany manganese dyskinesia in man.

Effect of stress on the response of rat brain to manganese.

Marked alterations in the contents of tyrosine, tryptophan,

, and norepinephrine in the brain tissue of rats after the combined treatment with immobilization and 

 suggested that the neurotoxic effects of the metal may be more pronounced in a stressful situation.

Manganese exposure during early larval stages of C. elegans causes learning disability in the adult stage.

 neurons showed resistance to neurodegeneration on repeated 

Dopamine alleviates salt-induced stress in Malus hupehensis.

In addition to changing stomatal behavior, supplementation with

 positively influenced the uptake of K, N, P, S, Cu and 

 ions but had an inhibitory effect on Na and Cl uptake, the balance of which is responsible for managing the response to salinity by Malus plants.

Mechanism of the manganese-catalyzed autoxidation of dopamine.

 through the formation of a highly reactive complex.

Manganese catalysis of dopamine oxidation.

 significantly increased the oxidation rate of 

, and the manganese complexes with some purines were especially efficient catalysts.

Manganese catalyzed auto-oxidation of dopamine to 6-hydroxydopamine in vitro.

 auto-oxidation could be linked mechanistically to the appearance of Mn-induced neurotoxic effects.

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Possible Interaction: Dopamine and Manganese

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