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Related Concept Videos

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...
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Single Cell Measurement of Dopamine Release with Simultaneous Voltage-clamp and Amperometry
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Published on: November 21, 2012

Amphetamine and methamphetamine reduce striatal dopamine transporter function without concurrent dopamine transporter

Christopher L German1, Glen R Hanson, Annette E Fleckenstein

  • 1Department of Pharmacology & Toxicology, University of Utah, Salt Lake City, Utah, USA.

Journal of Neurochemistry
|July 19, 2012
PubMed
Summary
This summary is machine-generated.

Amphetamine and methamphetamine alter dopamine transporter (DAT) function. In vivo studies show drug-induced DAT dysfunction occurs without changes in DAT localization, suggesting other mechanisms are involved.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Amphetamine (AMPH) and methamphetamine (METH) are psychostimulants known to affect dopamine transporter (DAT) function.
  • In vitro studies suggest AMPH-induced DAT internalization contributes to reduced DAT uptake, but in vivo evidence is limited.

Purpose of the Study:

  • To investigate the in vivo subcellular localization of DAT following AMPH and METH administration.
  • To determine if DAT relocalization contributes to acute and persistent DAT dysfunction.

Main Methods:

  • Developed a centrifugation technique to isolate striatal synaptosomal membrane and vesicle fractions.
  • Quantified DAT distribution within these fractions after in vivo AMPH/METH treatment.
  • Assessed DAT uptake and immunoreactivity.

Main Results:

  • In vitro, protein kinase C activation induced DAT internalization into vesicles.
  • In vivo, neither acute nor repeated AMPH/METH altered DAT localization in the short term, despite reduced uptake.
  • Repeated METH decreased total DAT immunoreactivity across all fractions after 7 days.

Conclusions:

  • DAT internalization is not the primary mechanism for acute DAT dysfunction after in vivo AMPH/METH.
  • Other factors likely contribute to DAT dysfunction and dopaminergic deficits.
  • Repeated METH causes a persistent decrease in total DAT levels.