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DNA of the impulsive but not the calm subjects was methylated at one DAT SNP.
nitrative damage accumulates in midbrain neurons with age; The capacity of a dopamine neuron to accumulate more cytosolic DA, as inferred from DA transporter expression, is related to accumulation of nitrative damage
Two C-terminal motifs dictate synaptic localization of DAT-1.
Endogenous dopamine actions in C. elegans are tightly regulated by synaptic DAT-1.
loss of UNC-64/DAT-1 interactions leads to enhanced synaptic dopamine release
Study generated a transgenic rat model that overexpresses the mouse DAT gene via pronuclear microinjection. These rats specifically exhibited behavioral and pharmaco-therapeutic phenotype of repetitive disorders. Together, findings suggest that the DAT rat model will constitute a valuable tool for studying the pathological role of DAT overexpression on neural systems relevant to relevant to neuropsychiatric disorders.
The findings of thuis study indicated that the DAT Val559 variant induces impulsivity behaviors that are dependent upon the reward context, with increased impulsive action observed when mice are required to delay responding for a reward.
These results suggest that DAT expression affects TH expression and phosphorylation largely in DA terminal field compartments.
These behavioral and molecular phenotypes indicate that a genetic-driven DAT hypofunction alters neurodevelopmental trajectories consistent with ADHD, but not with schizophrenia and bipolar disorders.
An exquisite microanatomical regulation of dopamine by the dopamine transporter was identified in striosomes relative to the matrix in the corpus striatum.
Data suggest that environment pollutants methylmercury and 1-methyl-4-phenylpyridinium decrease release of dopamine from dopaminergic neurons; this mechanism involves down-regulation of expression of Slc6a3.
This study show that Dopamine transporter is enriched in filopodia and induces filopodia formation.
The sigma-1R deficiency through suppressing NR2B (show GRIN2B Proteins) function and DAT expression can reduce MPTP (show PTPN2 Proteins)-induced death of dopaminergic neurons and parkinsonism.
DAT gene knockout in mice results dendritic spine loss in pyramidal neurons in the CA1 (show CA1 Proteins) field of the hippocampus.
Results show that moderate increases in DAT function cause spontaneous dopaminergic cell loss, oxidative stress and fine motor impairment that is reversed by l-DOPA treatment
DAT-mediated dopamine uptake plays a role in the absorption and distribution of dopamine following intranasal administration
SLC6A3 gene moderates the relation between maternal history of maltreatment and infant emotion regulation.
The age-related reduction in striatal DAT density also predicted memory decline, suggesting that a relation between striatal functions and memory decline in aging is multifaceted.
genetic association studies in population of young adults in Columbia: Data suggest that genetic polymorphisms in DRD4 (show DRD4 Proteins) and SLC6A3 are associated with overweight/obesity in the population studied; DRD4 (show DRD4 Proteins) 4/4 genotype is associated with lower BMI and SLC6A3 10/10 genotype is associated with higher BMI. (DRD4 (show DRD4 Proteins) = dopamine receptor D4 (show DRD4 Proteins); SLC6A3 = solute carrier family 6 member 3)
Results indicate that chronic coffee consumption in Parkinson's disease (PD) patients was not associated with significant change in striatal DAT availability, even after taking into account potentially confounding factors that are probably related to dopaminergic neuron decline (age, sex, disease duration, and severity of PD), treatment, and coffee-related habit (cigarette smoking).
This is the first study to investigate the association of rs3910105 in SNCA [SNCA protein, human] with DAT [dopamine transporter] availability. rs3910105 had an effect on DAT availability, and the correlation between DAT availability and SNCA transcripts were significant in CT [computed tomography] genotypes of rs3910105.
Study describes an association between the 6R6R genotype of the intron 8 VNTR of the dopamine transporter (DAT1) gene and crack cocaine addiction.
From all the statistically significant CpGs, methylation levels of cg00997378 (SLC6A3 gene) showed the highest differences (p < 0.0001), being associated with prematurity risk factors. SLC6A3 methylation, previously related to attention-deficit/hyperactivity disorder, neuronal function and behavior, might be a potential epigenetic biomarker with value in the early diagnosis and management of neurodevelopmenta
Results show that Gbetagamma activation regulates DAT activity by increasing dopamine (DA) efflux, and suggests that Gbetagamma promotes an efflux-willing state of the transporter and that the activation of a GPCR (show NMUR1 Proteins) can lead to a Gbetagamma-dependent DA efflux. Furthermore, the cellular responses that occur following activation of a Galphaq (show GNAQ Proteins)-coupled receptor are the result of multiple signaling pathways mediated by Galpha (show SUCLG1 Proteins)...
Findings demonstrate that histidine547 on hDAT plays a crucial role in stabilizing basal dopamine transport and Tat (show TAT Proteins)-DAT interaction.
In a study of the genetic association between polymorphisms in the DAT1, SERT (show SLC6A4 Proteins), COMT (show COMT Proteins) and BDNF (show BDNF Proteins) genes and attention deficit and hyperactive disorder, transmission disequilibrium test analysis showed that no individual allele of any variant studied has a preferential transmission.
This gene encodes a dopamine transporter which is a member of the sodium- and chloride-dependent neurotransmitter transporter family. The 3' UTR of this gene contains a 40 bp tandem repeat, referred to as a variable number tandem repeat or VNTR, which can be present in 3 to 11 copies. Variation in the number of repeats is associated with idiopathic epilepsy, attention-deficit hyperactivity disorder, dependence on alcohol and cocaine, susceptibility to Parkinson disease and protection against nicotine dependence.
dopamine transporter variant II
, sodium-dependent dopamine transporter
, solute carrier family 6 (neurotransmitter transporter, dopamine), member 3
, sodium-dependent dopamine transporter-like
, DA transporter
, dopamine transporter 1
, solute carrier family 6 member 3
, solute carrier family 6, member 3