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Dopamine is a hormone and neurotransmitter occurring in a wide variety of animals, including both vertebrates and invertebrates. In the brain, this phenethylamine functions as a neurotransmitter, activating the five types of dopamine receptors — D1, D2, D3, D4 and D5, and their variants. Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area.
Dopamine is also a neurohormone released by the hypothalamus. Its main function as a hormone is to inhibit the release of prolactin from the anterior lobe of the pituitary.

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Dopamine Research
Dopamine transporter inhibitory and antiparkinsonian effect of common flowering quince extract
Common flowering quince (FQ) is the fruit of Chaenomeles speciosa (Sweet) Nakai. FQ-containing cocktails have been applied to the treatment of neuralgia, migraine, and depression in traditional Chinese medicine. The present study assessed whether FQ is effective in dopamine transporter (DAT) regulation and antiparkinsonism by utilizing in vitro and in vivo assays, respectively. FQ at concentrations of 1–1000 μg/ml concentration-dependently inhibited dopamine uptake by Chinese hamster ovary (CHO) cells stably expressing DAT (D8 cells) and by synaptosomes. FQ had a slight inhibitory action on norepinephrine uptake by CHO cells expressing the norepinephrine transporter and no inhibitory effect on γ-aminobutyric acid (GABA) uptake by CHO cells expressing GABA transporter-1 or serotonin uptake by the serotonin transporter. A viability assay showed that FQ mitigated 1-methyl-4-phenylpyridinium-induced toxicity in D8 cells. Furthermore, in behavioral studies, FQ alleviated rotational behavior in 6-hydroxydopamine-treated rats and improved deficits in endurance performance in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. Furthermore, immunohistochemistry revealed that FQ markedly reduced the loss of tyrosine hydroxylase-positive neurons in the substantia nigra in MPTP-treated mice. In summary, FQ is a selective, potent DAT inhibitor and has antiparkinsonian-like effects that are mediated possibly by DAT suppression. FQ has the potential to be further developed for Parkinson's disease treatment.
Keywords: Common flowering quince; Parkinson's disease; Antiparkinsonism; Dopamine; Reuptake inhibitor; Transporter

NMDA receptor blockade augmented nicotine-evoked dopamine release from rat prefrontal cortex slices
Nicotine evokes dopamine release through activation of nicotinic acetylcholine receptors, and tobacco cigarette smoking is more prevalent among individuals diagnosed with schizophrenia. Blockade of ionotropic glutamate (NMDA) receptors can induce changes in central dopamine and glutamate circuits, which models the symptoms of schizophrenia. The effect of the NMDA receptor antagonist, ketamine, on the effect of nicotine in rat prefrontal cortex was examined using a slice superfusion assay in which cortical slices were preloaded with [3H] dopamine. A wide range of ketamine concentrations (0.1–300 μM) did not evoke [3H] overflow from slices, indicating that NMDA receptor blockade did not induce dopamine release. Ketamine, at concentrations that model the symptoms of schizophrenia (1–10 μM), augmented the effect of nicotine (1–100 μM) to evoke [3H] overflow from slices and decreased the threshold nicotine concentration to evoke [3H] overflow. This indicates that NMDA receptor blockade increased the potency and efficacy of nicotine to evoke dopamine release from prefrontal cortex slices, suggesting that ketamine induced hypersensitivity to nicotine. The present results support a role for nicotinic acetylcholine receptors in the pathophysiology and treatment of schizophrenia.
Keywords: Schizophrenia; Nicotine; Ketamine; Dopamine; Glutamate; NMDA

PI3K signaling supports amphetamine-induced dopamine efflux
The dopamine (DA) transporter (DAT) is a major molecular target of the psychostimulant amphetamine (AMPH). AMPH, as a result of its ability to reverse DAT-mediated inward transport of DA, induces DA efflux thereby increasing extracellular DA levels. This increase is thought to underlie the behavioral effects of AMPH. We have demonstrated previously that insulin, through phosphatidylinositol 3-kinase (PI3K) signaling, regulates DA clearance by fine-tuning DAT plasma membrane expression. PI3K signaling may represent a novel mechanism for regulating DA efflux evoked by AMPH, since only active DAT at the plasma membrane can efflux DA. Here, we show in both a heterologous expression system and DA neurons that inhibition of PI3K decreases DAT cell surface expression and, as a consequence, AMPH-induced DA efflux.
Keywords: Dopamine transporter (DAT); Amphetamine (AMPH); Dopamine (DA); Phosphatidylinositol 3-kinase (PI3K); Insulin; Drug abuse; Transient current

A thermodynamic investigation on quenching mechanisms of the singlet and triplet state riboflavin by dopamine
The quenching mechanisms of both the singlet and triplet state riboflavin (RF) by dopamine (DP) were investigated by means of density functional theory calculations in this communication. It was found that both the direct electron transfer and H-atom transfer pathways are thermodynamically feasible for the singlet state RF quenching by DP, while only the H-atom transfer pathway is involved in the triplet state RF quenching by DP.
Keywords: Dopamine; Riboflavin; Excited state; Quenching mechanism; Density functional theory

Behavioral abnormalities and dopamine reductions in sdy mutant mice with a deletion in Dtnbp1, a susceptibility gene for schizophrenia
Genetic susceptibility plays an important role in the pathogenesis of schizophrenia. Genetic evidence for an association between the dysbindin-1 gene (DTNBP1: dystrobrevin binding protein 1) and schizophrenia has been repeatedly reported in various populations worldwide. Thus, we performed behavioral analyses on homozygous sandy (sdy) mice, which lack dysbindin-1 owing to a deletion in the Dtnbp1 gene. Our results showed that sdy mice were less active and spent less time in the center of an open field apparatus. Consistent with the latter observation, sdy mice also displayed evidence of heightened anxiety-like response and deficits in social interaction. Compared to wild-type mice, sdy mice displayed lower levels of dopamine, but not glutamate, in the cerebral cortex, hippocampus, and hypothalamus. These findings indicate that sdy mice display a number of behavioral abnormalities associated with schizophrenia and suggest that these abnormalities may be mediated by reductions in forebrain dopamine transmission.
Keywords: Schizophrenia; Dysbindin-1; Locomotor activity; Anxiety; Dopamine; Endophenotype

Antagonizing dopamine D1-like receptor inhibits Th17 cell differentiation: Preventive and therapeutic effects on experimental autoimmune encephalomyelitis
Five types of dopamine receptors, termed D1 to D5, have been identified to date. The D1 and D5 receptors form the D1-like group that couples with the Gs class of G proteins, while D2, D3 and D4 form the D2-like group that couples with the Gi class of G proteins. A D2-like-receptor (D2-like-R) antagonist L750667 induced dendritic cell (DC)-mediated Th17 differentiation. In contrast, a D1-like-R antagonist SCH23390 inhibited DC-mediated Th17 differentiation. The D1-like-Rs were expressed on both DCs and T cells, whereas D2-like-Rs were marginally expressed on CD4+CD45RA+ naïve T cells. In addition, SCH23390 had the ability to prevent experimental autoimmune encephalomyelitis (EAE) in mice. Spleen cells from EAE mice showed decreased IL-17 production, when SCH23390 was administered. Adoptive transfer of DCs treated with SCH23390 successfully prevented EAE. These findings indicate that antagonizing D1-like-Rs on DCs inhibits Th17 differentiation, thereby leading to an amelioration of EAE.
Keywords: Dopamine receptor; Dendritic cell; Experimental autoimmune encephalomyelitis; Th17; D1-like-R antagonist; D2-like-R antagonist

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