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Human Dopaminergic sentence examples within induced pluripotent stem

induced pluripotent stem

Cultures of isogenic induced pluripotent stem cell (iPSC) lines with and without PARK2 knockout (KO) enable mechanistic studies of the effect of parkin deficiency in human dopaminergic neurons.

Lysosomal perturbations in dopaminergic neurons derived from induced pluripotent stem cells with PARK2 mutation

induced pluripotent stem

Measurements on these biosensors expressed in Neuro2a cells and in human dopaminergic neurons differentiated from induced pluripotent stem cells (iPSCs) show that S-ketamine enters the ER within a few seconds after appearing in the external solution near the PM, then leaves as rapidly after S-ketamine is removed from the extracellular solution.

Biosensors Show the Pharmacokinetics of S-Ketamine in the Endoplasmic Reticulum

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Human Dopaminergic sentence examples within Protect Human Dopaminergic

Protect Human Dopaminergic

In dopamine toxicity studies, wild-type parkin, but not disease-linked mutants, protects human dopaminergic cells, in part through lowering H2O2.

Age-associated insolubility of parkin in human midbrain is linked to redox balance and sequestration of reactive dopamine metabolites

Protect Human Dopaminergic

Moreover, pharmacological activation of macroautophagy via diverse signaling pathways is effective to protect human dopaminergic neurons against alpha‐synuclein‐induced toxicity.

Multiple molecular pathways stimulating macroautophagy protect from alpha-synuclein-induced toxicity in human neurons

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Human Dopaminergic sentence examples within human dopaminergic neuron

human dopaminergic neuron

RNF11 expression decreases in human dopaminergic neurons during PD, and that decrease may be protective by increasing dopamine neurotransmission in the surviving dopaminergic neurons.

Ring Finger Protein 11 (RNF11) Modulates Dopamine Release in Drosophila

human dopaminergic neuron

We previously identified a genetic risk variant for cocaine addiction in the PLCB1 gene and found this gene upregulated in postmortem brains of cocaine abusers and in human dopaminergic neuron-like cells after an acute cocaine exposure.

Reduced cue-induced reinstatement of cocaine-seeking behavior in Plcb1 +/− mice

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Human Dopaminergic sentence examples within human dopaminergic neuroblastoma

human dopaminergic neuroblastoma

In this context, the present study aimed to evaluate the antioxidant activity of CMI in H2O2-induced oxidative stress on human dopaminergic neuroblastoma cells (SH-SY5Y) and to shed some light into its possible mechanism of action.

Neuroprotective Effect of 3-[(4-Chlorophenyl)selanyl]-1-methyl-1H-indole on Hydrogen Peroxide-Induced Oxidative Stress in SH-SY5Y Cells.

human dopaminergic neuroblastoma

In this study, we characterized the toxic mechanism and possible protective compounds against TMT-induced neurotoxicity in human dopaminergic neuroblastoma SH-SY5Y cells.

Inhibitors of Lipoxygenase and Cyclooxygenase-2 Attenuate Trimethyltin-Induced Neurotoxicity through Regulating Oxidative Stress and Pro-Inflammatory Cytokines in Human Neuroblastoma SH-SY5Y Cells

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Human Dopaminergic sentence examples within human dopaminergic sh

human dopaminergic sh

Here, we investigated whether T-I would be able to prevent the consequences resulting from the exposure of the human dopaminergic SH-SY5Y cells to CPF.

Suppression of Mitochondria-Related Bioenergetics Collapse and Redox Impairment by Tanshinone I, a Diterpenoid Found in Salvia miltiorrhiza Bunge (Danshen), in the Human Dopaminergic SH-SY5Y Cell Line Exposed to Chlorpyrifos.

human dopaminergic sh

Rutin is a bioflavonoid with multiple pharmacological effects, and this study investigated the neuroprotective effects of rutin in the human dopaminergic SH-SY5Y cell line using the neurotoxin MPP+.

Inhibition of γH2AX, COX-2 and regulation of antioxidant enzymes in MPP+-exposed SH-SY5Y cells pre-treated with rutin.

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Human Dopaminergic sentence examples within human dopaminergic cell

human dopaminergic cell

In dopamine toxicity studies, wild-type parkin, but not disease-linked mutants, protects human dopaminergic cells, in part through lowering H2O2.

Age-associated insolubility of parkin in human midbrain is linked to redox balance and sequestration of reactive dopamine metabolites

human dopaminergic cell

Herein, we show that a number of lncRNA genes encompassing transcriptional units in close proximity to PD-linked protein-coding genes, including SNCA, LRRK2, PINK1, DJ-1, UCH-L1, MAPT and GBA1, are expressed in human dopaminergic cells and post-mortem material, such as cortex, Substantia Nigra and cerebellum.

Long Non-coding RNAs Associated With Neurodegeneration-Linked Genes Are Reduced in Parkinson’s Disease Patients

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Human Dopaminergic sentence examples within human dopaminergic system

human dopaminergic system

Our work highlights the flexibility of the human dopaminergic system, which can enhance memory formation not only through explicit and/or primary reinforcers but also via abstract and aesthetic rewards such as music.

Dopamine modulations of reward‐driven music memory consolidation

human dopaminergic system

Based on these findings, we used fMRI to assess changes in spontaneous neural activity strength in the human dopaminergic system after prefrontal tDCS compared with the administration of the dopamine precursor and standard anti-Parkinson drug levodopa (l-DOPA).

Increased Neural Activity in Mesostriatal Regions after Prefrontal Transcranial Direct Current Stimulation and l-DOPA Administration

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Human Dopaminergic sentence examples within human dopaminergic neuronal

human dopaminergic neuronal

Starting with a comprehensive generic reconstruction of human metabolism, Recon3D, we generated a high-quality, constraint-based, genome-scale, in silico model of human dopaminergic neuronal metabolism (iDopaNeuro1).

Mechanistic model-driven exometabolomic characterisation of human dopaminergic neuronal metabolism

human dopaminergic neuronal

Five cI, three complex II (cII), and five complex III (cIII) inhibitors were characterized in detail in human dopaminergic neuronal cell cultures.

Neurotoxicity and underlying cellular changes of 21 mitochondrial respiratory chain inhibitors

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10.3389/fncel.2019.00058

Herein, we show that a number of lncRNA genes encompassing transcriptional units in close proximity to PD-linked protein-coding genes, including SNCA, LRRK2, PINK1, DJ-1, UCH-L1, MAPT and GBA1, are expressed in human dopaminergic cells and post-mortem material, such as cortex, Substantia Nigra and cerebellum.

Long Non-coding RNAs Associated With Neurodegeneration-Linked Genes Are Reduced in Parkinson’s Disease Patients

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10.1080/14786419.2019.1689503

All compounds were evaluated for their neuroprotective effects against H2O2-induced damage in human dopaminergic neuroblastoma cells (SH-SY5Y).

A new monoterpene-lactone with neuroprotective activity from corn silk.

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10.1007/s11033-019-05037-6

We examined the effects of AAE on rotenone-induced mitochondrial complex I dysfunction in human dopaminergic SH-SY5Y cells.

Araucaria angustifolia (Bertol.) Kuntze has neuroprotective action through mitochondrial modulation in dopaminergic SH-SY5Y cells

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10.1002/jcb.27865

Taken together, these results demonstrate that upregulated lncRNA SNHG1 promotes MPP+‐induced cytotoxicity and ROS production through the miR‐15b‐5p/GSK3β axis in human dopaminergic SH‐SY5Y cells, suggesting that SNHG1 may act as a potential therapeutic target for PD treatment in the future.

Upregulated lncRNA small nucleolar RNA host gene 1 promotes 1‐methyl‐4‐phenylpyridinium ion‐induced cytotoxicity and reactive oxygen species production through miR‐15b‐5p/GSK3β axis in human dopaminergic SH‐SY5Y cells

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10.1007/s12035-019-01745-z

Our results show that PDE7 is upregulated after an injury both in the human dopaminergic cell line SH-SY5Y and in primary rat mesencephalic cultures and after lipopolysaccharide or 6-hidroxydopamine injection in the Substantia nigra pars compacta of adult mice.

Phosphodiesterase 7 Regulation in Cellular and Rodent Models of Parkinson’s Disease

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10.1016/j.bcp.2019.02.019

We found, in fact, that HyNDA‐1 significantly modulated structural plasticity on both mice and human dopaminergic neurons, an effect strongly prevented by co‐incubating this ligand with either nAChR or D3R antagonists.

The novel hybrid agonist HyNDA‐1 targets the D3R‐nAChR heteromeric complex in dopaminergic neurons

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10.1007/s00204-019-02497-4

To deepen our knowledge of the biochemical disturbances resulting from U(VI) toxicity in neuronal cells, two complementary strategies were set up to identify the proteins that selectively bind U(VI) in human dopaminergic SH-SY5Y cells.

Deciphering the uranium target proteins in human dopaminergic SH-SY5Y cells

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10.1002/ps.5559

Lastly, the cytotoxicity data of pyrethroids on human dopaminergic neuroblastoma SH-SY5Y cells confirms that the synthesized compounds are low toxic to the cells.

Synthesis, Insecticidal Activities, Resistance in Aedes albopictus and Cytotoxicity of Novel Dihaloacetylated Heterocyclic Pyrethroids.

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10.1177/2470547019842545

Human dopaminergic neurons were differentiated from inducible pluripotent stem cells for over 60 days.

Structural Plasticity Induced by Ketamine in Human Dopaminergic Neurons as Mechanism Relevant for Treatment-Resistant Depression

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10.1089/rej.2018.2062

In this study, we investigated the effects of abscisic acid (ABA) on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in human dopaminergic neuroblastoma SH-SY5Y cell line as an in vitro model of PD.

Phytohormone Abscisic Acid Protects Human Neuroblastoma SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Neurotoxicity Through Its Antioxidant and Antiapoptotic Properties.

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10.1073/pnas.1910061116

Using the BRAVE approach and hidden Markov model-based clustering, we present 25 synthetic capsid variants with refined properties, such as retrograde axonal transport in specific subtypes of neurons, as shown for both rodent and human dopaminergic neurons.

A systematic capsid evolution approach performed in vivo for the design of AAV vectors with tailored properties and tropism

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10.1523/JNEUROSCI.3128-18.2019

Based on these findings, we used fMRI to assess changes in spontaneous neural activity strength in the human dopaminergic system after prefrontal tDCS compared with the administration of the dopamine precursor and standard anti-Parkinson drug levodopa (l-DOPA).

Increased Neural Activity in Mesostriatal Regions after Prefrontal Transcranial Direct Current Stimulation and l-DOPA Administration

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10.1523/JNEUROSCI.3085-18.2019

Together, these results suggest that intracellular α-syn levels are regulated by lysosomal exocytosis in human dopaminergic neurons and may represent a potential therapeutic target for PD and other synucleinopathies.

Increased Lysosomal Exocytosis Induced by Lysosomal Ca2+ Channel Agonists Protects Human Dopaminergic Neurons from α-Synuclein Toxicity

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10.3390/jfb10030032

Human dopaminergic neurons were differentiated from neural precursor cells and characterized by electrophysiological and immune histochemical methods.

Novel Tools towards Magnetic Guidance of Neurite Growth: (I) Guidance of Magnetic Nanoparticles into Neurite Extensions of Induced Human Neurons and In Vitro Functionalization with RAS Regulating Proteins

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10.5487/TR.2019.35.1.083

Previously, we found that zinc oxide (ZnO) NPs that are neurotoxic to human dopaminergic neuroblastoma SH-SY5Y cells are mediated by lipoxygenase (LOX), not cyclooxygenase-2 (COX-2).

Zinc Oxide Nanoparticles Exhibit Both Cyclooxygenase- and Lipoxygenase-Mediated Apoptosis in Human Bone Marrow-Derived Mesenchymal Stem Cells

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10.1016/j.neulet.2019.134287

This study investigates whether METH induces autophagy in the human dopaminergic neuroblastoma cell line SH-SY5Y, then examines the neuroprotective effects of gastrodin against autophagy in METH-treated SH-SY5Y cells.

Protective effect of gastrodin against methamphetamine-induced autophagy in human dopaminergic neuroblastoma SH-SY5Y cells via the AKT/mTOR signaling pathway

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10.1016/j.euroneuro.2017.08.422

We observed a significant upregulation of PLCB1 in the nucleus accumbens of cocaine abusers and in human dopaminergic-like neurons after cocaine treatment.

M115: ASSOCIATION OF THE PLCB1 GENE WITH DRUG DEPENDENCE

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10.1007/s11910-019-0925-z

Particularly, no genome-wide αSyn toxicity screen in human dopaminergic neurons has been published so far.

Unbiased Screens for Modifiers of Alpha-Synuclein Toxicity

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Human Dopaminergic
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What is/are Human Dopaminergic?

Human Dopaminergic - Herein, we show that a number of lncRNA genes encompassing transcriptional units in close proximity to PD-linked protein-coding genes, including SNCA, LRRK2, PINK1, DJ-1, UCH-L1, MAPT and GBA1, are expressed in human dopaminergic cells and post-mortem material, such as cortex, Substantia Nigra and cerebellum. [1] All compounds were evaluated for their neuroprotective effects against H2O2-induced damage in human dopaminergic neuroblastoma cells (SH-SY5Y). [2] We examined the effects of AAE on rotenone-induced mitochondrial complex I dysfunction in human dopaminergic SH-SY5Y cells. [3] Taken together, these results demonstrate that upregulated lncRNA SNHG1 promotes MPP+‐induced cytotoxicity and ROS production through the miR‐15b‐5p/GSK3β axis in human dopaminergic SH‐SY5Y cells, suggesting that SNHG1 may act as a potential therapeutic target for PD treatment in the future. [4] Our results show that PDE7 is upregulated after an injury both in the human dopaminergic cell line SH-SY5Y and in primary rat mesencephalic cultures and after lipopolysaccharide or 6-hidroxydopamine injection in the Substantia nigra pars compacta of adult mice. [5] We found, in fact, that HyNDA‐1 significantly modulated structural plasticity on both mice and human dopaminergic neurons, an effect strongly prevented by co‐incubating this ligand with either nAChR or D3R antagonists. [6] To deepen our knowledge of the biochemical disturbances resulting from U(VI) toxicity in neuronal cells, two complementary strategies were set up to identify the proteins that selectively bind U(VI) in human dopaminergic SH-SY5Y cells. [7] Lastly, the cytotoxicity data of pyrethroids on human dopaminergic neuroblastoma SH-SY5Y cells confirms that the synthesized compounds are low toxic to the cells. [8] Human dopaminergic neurons were differentiated from inducible pluripotent stem cells for over 60 days. [9] In this study, we investigated the effects of abscisic acid (ABA) on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in human dopaminergic neuroblastoma SH-SY5Y cell line as an in vitro model of PD. [10] Using the BRAVE approach and hidden Markov model-based clustering, we present 25 synthetic capsid variants with refined properties, such as retrograde axonal transport in specific subtypes of neurons, as shown for both rodent and human dopaminergic neurons. [11] Based on these findings, we used fMRI to assess changes in spontaneous neural activity strength in the human dopaminergic system after prefrontal tDCS compared with the administration of the dopamine precursor and standard anti-Parkinson drug levodopa (l-DOPA). [12] Together, these results suggest that intracellular α-syn levels are regulated by lysosomal exocytosis in human dopaminergic neurons and may represent a potential therapeutic target for PD and other synucleinopathies. [13] Human dopaminergic neurons were differentiated from neural precursor cells and characterized by electrophysiological and immune histochemical methods. [14] Previously, we found that zinc oxide (ZnO) NPs that are neurotoxic to human dopaminergic neuroblastoma SH-SY5Y cells are mediated by lipoxygenase (LOX), not cyclooxygenase-2 (COX-2). [15] This study investigates whether METH induces autophagy in the human dopaminergic neuroblastoma cell line SH-SY5Y, then examines the neuroprotective effects of gastrodin against autophagy in METH-treated SH-SY5Y cells. [16] We observed a significant upregulation of PLCB1 in the nucleus accumbens of cocaine abusers and in human dopaminergic-like neurons after cocaine treatment. [17] Particularly, no genome-wide αSyn toxicity screen in human dopaminergic neurons has been published so far. [18]

induced pluripotent stem

Cultures of isogenic induced pluripotent stem cell (iPSC) lines with and without PARK2 knockout (KO) enable mechanistic studies of the effect of parkin deficiency in human dopaminergic neurons. [1] Measurements on these biosensors expressed in Neuro2a cells and in human dopaminergic neurons differentiated from induced pluripotent stem cells (iPSCs) show that S-ketamine enters the ER within a few seconds after appearing in the external solution near the PM, then leaves as rapidly after S-ketamine is removed from the extracellular solution. [2] In this study, we used self-assembling peptide nanofiber scaffolds (SAPNS) based on the peptide RADA16-I to support the in vitro maturation and in vivo post-transplantation survival of encapsulated human dopaminergic (DA) neurons derived from induced pluripotent stem cells (iPSCs). [3] Induced pluripotent stem cells (iPSCs) differentiated toward a dopaminergic neuronal phenotype offer a valuable source to generate human dopaminergic neurons. [4] By using the proximity ligation assay, we have shown that the D3R-nAChR heteromer is also expressed in human dopaminergic neurons derived from induced pluripotent stem cells. [5]

Protect Human Dopaminergic

In dopamine toxicity studies, wild-type parkin, but not disease-linked mutants, protects human dopaminergic cells, in part through lowering H2O2. [1] Moreover, pharmacological activation of macroautophagy via diverse signaling pathways is effective to protect human dopaminergic neurons against alpha‐synuclein‐induced toxicity. [2]

human dopaminergic neuron

RNF11 expression decreases in human dopaminergic neurons during PD, and that decrease may be protective by increasing dopamine neurotransmission in the surviving dopaminergic neurons. [1] We previously identified a genetic risk variant for cocaine addiction in the PLCB1 gene and found this gene upregulated in postmortem brains of cocaine abusers and in human dopaminergic neuron-like cells after an acute cocaine exposure. [2] The same finding was replicated in an in vivo mouse model of templated α-syn aggregation and in human dopaminergic neurons, suggesting that PLK2 is more likely to be involved in S129-phosphorylation of the soluble physiological fraction of α-syn. [3] Our work provides a unique resource of transcription factors and regulatory elements, potentially involved in the acquisition of human dopaminergic neuron cell identity. [4] Objectives To identify genome-wide DNA methylation and hydroxymethylation changes induced by overexpression of two alpha-synuclein variants in human dopaminergic neurons, and to relate these to the corresponding transcriptome. [5] The same finding was replicated in an in-vivo mouse models of templated α-syn aggregation and human dopaminergic neurons, suggesting that PLK2 is more likely to be involved in S129 phosphorylation of soluble non-pathology related fraction of α-syn. [6] Methods Human dopaminergic neuron-like cells (differentiated SH-SY5Y cells) were treated with rotenone in the presence or absence of the LRRK2 kinase inhibitor GSK2578215A (GSK-KI) for 48 h. [7] The α-Syn/p25α strain induced larger inclusions in human dopaminergic neurons. [8] α-Synuclein is critical in the pathogenesis of Parkinson’s disease and related disorders, yet it remains unclear how its aggregation causes degeneration of human dopaminergic neurons. [9] However, due to the complexity of PB-II and the difficulty of culturing human dopaminergic neurons (DAn) in vitro, the mechanism of PB-II to treat PD remains unclear. [10] Cultures of isogenic induced pluripotent stem cell (iPSC) lines with and without PARK2 knockout (KO) enable mechanistic studies of the effect of parkin deficiency in human dopaminergic neurons. [11] We found, in fact, that HyNDA‐1 significantly modulated structural plasticity on both mice and human dopaminergic neurons, an effect strongly prevented by co‐incubating this ligand with either nAChR or D3R antagonists. [12] Human dopaminergic neurons were differentiated from inducible pluripotent stem cells for over 60 days. [13] Measurements on these biosensors expressed in Neuro2a cells and in human dopaminergic neurons differentiated from induced pluripotent stem cells (iPSCs) show that S-ketamine enters the ER within a few seconds after appearing in the external solution near the PM, then leaves as rapidly after S-ketamine is removed from the extracellular solution. [14] Therefore, we investigated deleterious effects of mitochondria-targeted aSYN in differentiated human dopaminergic neurons in comparison with wild-type (WT) aSYN overexpression and corresponding EGFP (enhanced green fluorescent protein)-expressing controls. [15] Moreover, pharmacological activation of macroautophagy via diverse signaling pathways is effective to protect human dopaminergic neurons against alpha‐synuclein‐induced toxicity. [16] Using the BRAVE approach and hidden Markov model-based clustering, we present 25 synthetic capsid variants with refined properties, such as retrograde axonal transport in specific subtypes of neurons, as shown for both rodent and human dopaminergic neurons. [17] Together, these results suggest that intracellular α-syn levels are regulated by lysosomal exocytosis in human dopaminergic neurons and may represent a potential therapeutic target for PD and other synucleinopathies. [18] Human dopaminergic neurons were differentiated from neural precursor cells and characterized by electrophysiological and immune histochemical methods. [19] Induced pluripotent stem cells (iPSCs) differentiated toward a dopaminergic neuronal phenotype offer a valuable source to generate human dopaminergic neurons. [20] Particularly, no genome-wide αSyn toxicity screen in human dopaminergic neurons has been published so far. [21] By using the proximity ligation assay, we have shown that the D3R-nAChR heteromer is also expressed in human dopaminergic neurons derived from induced pluripotent stem cells. [22]

human dopaminergic neuroblastoma

In this context, the present study aimed to evaluate the antioxidant activity of CMI in H2O2-induced oxidative stress on human dopaminergic neuroblastoma cells (SH-SY5Y) and to shed some light into its possible mechanism of action. [1] In this study, we characterized the toxic mechanism and possible protective compounds against TMT-induced neurotoxicity in human dopaminergic neuroblastoma SH-SY5Y cells. [2] All compounds were evaluated for their neuroprotective effects against H2O2-induced damage in human dopaminergic neuroblastoma cells (SH-SY5Y). [3] Lastly, the cytotoxicity data of pyrethroids on human dopaminergic neuroblastoma SH-SY5Y cells confirms that the synthesized compounds are low toxic to the cells. [4] In this study, we investigated the effects of abscisic acid (ABA) on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in human dopaminergic neuroblastoma SH-SY5Y cell line as an in vitro model of PD. [5] Previously, we found that zinc oxide (ZnO) NPs that are neurotoxic to human dopaminergic neuroblastoma SH-SY5Y cells are mediated by lipoxygenase (LOX), not cyclooxygenase-2 (COX-2). [6] This study investigates whether METH induces autophagy in the human dopaminergic neuroblastoma cell line SH-SY5Y, then examines the neuroprotective effects of gastrodin against autophagy in METH-treated SH-SY5Y cells. [7]

human dopaminergic sh

Here, we investigated whether T-I would be able to prevent the consequences resulting from the exposure of the human dopaminergic SH-SY5Y cells to CPF. [1] Rutin is a bioflavonoid with multiple pharmacological effects, and this study investigated the neuroprotective effects of rutin in the human dopaminergic SH-SY5Y cell line using the neurotoxin MPP+. [2] We examined the effects of AAE on rotenone-induced mitochondrial complex I dysfunction in human dopaminergic SH-SY5Y cells. [3] Taken together, these results demonstrate that upregulated lncRNA SNHG1 promotes MPP+‐induced cytotoxicity and ROS production through the miR‐15b‐5p/GSK3β axis in human dopaminergic SH‐SY5Y cells, suggesting that SNHG1 may act as a potential therapeutic target for PD treatment in the future. [4] To deepen our knowledge of the biochemical disturbances resulting from U(VI) toxicity in neuronal cells, two complementary strategies were set up to identify the proteins that selectively bind U(VI) in human dopaminergic SH-SY5Y cells. [5]

human dopaminergic cell

In dopamine toxicity studies, wild-type parkin, but not disease-linked mutants, protects human dopaminergic cells, in part through lowering H2O2. [1] Herein, we show that a number of lncRNA genes encompassing transcriptional units in close proximity to PD-linked protein-coding genes, including SNCA, LRRK2, PINK1, DJ-1, UCH-L1, MAPT and GBA1, are expressed in human dopaminergic cells and post-mortem material, such as cortex, Substantia Nigra and cerebellum. [2] Our results show that PDE7 is upregulated after an injury both in the human dopaminergic cell line SH-SY5Y and in primary rat mesencephalic cultures and after lipopolysaccharide or 6-hidroxydopamine injection in the Substantia nigra pars compacta of adult mice. [3]

human dopaminergic system

Our work highlights the flexibility of the human dopaminergic system, which can enhance memory formation not only through explicit and/or primary reinforcers but also via abstract and aesthetic rewards such as music. [1] Based on these findings, we used fMRI to assess changes in spontaneous neural activity strength in the human dopaminergic system after prefrontal tDCS compared with the administration of the dopamine precursor and standard anti-Parkinson drug levodopa (l-DOPA). [2]

human dopaminergic neuronal

Starting with a comprehensive generic reconstruction of human metabolism, Recon3D, we generated a high-quality, constraint-based, genome-scale, in silico model of human dopaminergic neuronal metabolism (iDopaNeuro1). [1] Five cI, three complex II (cII), and five complex III (cIII) inhibitors were characterized in detail in human dopaminergic neuronal cell cultures. [2]