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Related Concept Videos

Human Genetics01:28

Human Genetics

Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
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Pharmacogenetics of Drug Metabolism: Overview

Genetic polymorphism in drug metabolism is crucial to the inter-individual variability observed in drug responses. Drug metabolism primarily involves the chemical modification of drugs and other xenobiotics to enhance their elimination by increasing their polarity. Two main classes of enzymes mediate this biotransformation process: Phase I enzymes, primarily cytochrome P450s, catalyze oxidation and reduction reactions, while other enzymes, such as esterases, mediate hydrolysis, and Phase II...

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Related Experiment Video

Updated: May 27, 2026

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area
09:54

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area

Published on: August 10, 2012

Dopamine effects on human error processing depend on catechol-O-methyltransferase VAL158MET genotype.

Erik M Mueller1, Scott Makeig, Gerhard Stemmler

  • 1Philipps-Universität Marburg, 35032 Marburg, Germany. erik.mueller@staff.uni-marburg.de

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|November 4, 2011
PubMed
Summary

Brain dopamine levels influence error processing. Both low and high dopamine, modulated by COMT genotype and a D2 receptor blocker, enhance error-related brain activity and subsequent performance adjustments.

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Assessment of Dopaminergic Homeostasis in Mice by Use of High-performance Liquid Chromatography Analysis and Synaptosomal Dopamine Uptake
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Assessment of Dopaminergic Homeostasis in Mice by Use of High-performance Liquid Chromatography Analysis and Synaptosomal Dopamine Uptake

Published on: September 21, 2017

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Last Updated: May 27, 2026

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area
09:54

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area

Published on: August 10, 2012

Assessment of Dopaminergic Homeostasis in Mice by Use of High-performance Liquid Chromatography Analysis and Synaptosomal Dopamine Uptake
11:26

Assessment of Dopaminergic Homeostasis in Mice by Use of High-performance Liquid Chromatography Analysis and Synaptosomal Dopamine Uptake

Published on: September 21, 2017

Area of Science:

  • Neuroscience
  • Cognitive Neuroscience
  • Psychopharmacology

Background:

  • Dopamine (DA) in the prefrontal cortex (PFC) is implicated in error processing.
  • The catechol-O-methyltransferase (COMT) Val158Met polymorphism affects PFC DA levels, with Val allele linked to lower DA.
  • D2 receptor availability and serotonin transporter function may also modulate DA's role in cognitive control.

Purpose of the Study:

  • To investigate the hypothesis that high and low prefrontal cortex (PFC) dopamine levels enhance error-specific neural activity and behavioral adjustments.
  • To examine the interaction between COMT genotype, D2 receptor blockade, and error processing.
  • To explore the influence of serotonin transporter genetics on these relationships.

Main Methods:

  • 169 male participants were genotyped for COMT Val158Met, DRD2TaqIa, and 5-HTTLPR.
  • Participants received a placebo or a D2 receptor antagonist (sulpiride).
  • Electroencephalography (EEG) was used during a Flanker task to analyze error-related negativity (ERN), midcingulate cortex power, and post-error slowing (PES).

Main Results:

  • Errors elicited increased IC-ERN, delta/theta power in the midcingulate cortex, and post-error slowing (PES).
  • COMT genotype interacted with sulpiride administration: the Val allele (lower PFC DA) predicted higher IC-ERN, delta/theta power, and PES under placebo, an effect reversed by sulpiride.
  • These effects were further modulated by the 5-HTTLPR genotype, suggesting serotonin's influence.

Conclusions:

  • Both low (Val allele, placebo) and high (Met allele, sulpiride) PFC DA levels enhance error-related neural signals and behavioral adjustments compared to medium levels.
  • This U-shaped relationship between PFC DA and error processing highlights the complex role of dopamine in cognitive control.
  • Serotonin system genetics interact with dopamine pathways to fine-tune error monitoring and performance regulation.