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Updated: Jun 12, 2026
10:04
Local Application of Drugs to Study Nicotinic Acetylcholine Receptor Function in Mouse Brain Slices
Published on: October 29, 2012
Enhanced dopamine transporter function in striatum during nicotine withdrawal
Maria Hadjiconstantinou1, Anne-Marie Duchemin, Hailing Zhang
1Department of Psychiatry, Division of Molecular Neuropsychopharmacology, The Ohio Sate University College of Medicine, Columbus, Ohio 43210, USA.
Synapse (New York, N.Y.)
|May 28, 2010
Summary
Nicotine withdrawal increases dopamine transporter (DAT) function in the brain, leading to lower dopamine levels. This enhanced DAT activity may contribute to the mood changes experienced during nicotine cessation.
Area of Science:
- Neuroscience
- Pharmacology
- Addiction Research
Background:
- Nicotine withdrawal is linked to dopamine deficits in the striatum, potentially causing affective symptoms.
- Dopamine transporter (DAT) regulates extracellular dopamine levels, making it a potential factor in withdrawal.
Purpose of the Study:
- To investigate alterations in DAT expression and function within the striatum during nicotine withdrawal.
Main Methods:
- Male mice received daily nicotine injections for 14 days, followed by withdrawal periods of 4-72 hours.
- Assessed dopamine uptake in striatal synaptosomes and DAT mRNA levels via in situ hybridization.
- Measured endogenous dopamine overflow in striatal slices and the effect of a DAT inhibitor.
Main Results:
- Dopamine uptake into striatal synaptosomes increased 12-24 hours post-nicotine discontinuation.
- Elevated DAT mRNA levels were observed in the substantia nigra and ventral tegmental area.
- Decreased extracellular dopamine overflow in the striatum paralleled increased DAT function.
Conclusions:
- The dopamine transporter (DAT) is transiently upregulated in the striatum early in nicotine withdrawal.
- Enhanced DAT function contributes to reduced extracellular dopamine levels during nicotine cessation.
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