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Monoamine transporters: from genes to behavior
Raul R Gainetdinov1, Marc G Caron
1Howard Hughes Medical Institute Laboratories, Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA. r.gainetdinov@cellbio.duke.edu
Annual Review of Pharmacology and Toxicology
|October 3, 2002
Summary
Genetic mouse models lacking monoamine transporters (dopamine transporter, serotonin transporter, and norepinephrine transporter) are crucial for understanding neurotransmission. These models help elucidate transporter roles in physiology, pathology, and drug action.
Area of Science:
- Neuroscience
- Pharmacology
- Genetics
Background:
- Monoamine transporters (dopamine transporter, serotonin transporter, norepinephrine transporter) regulate neurotransmission and are targets for various drugs.
- Understanding their function is vital for numerous physiological and pathological conditions.
Purpose of the Study:
- To review recent advances in understanding monoamine transporter physiology and pharmacology.
- To highlight the utility of genetically modified mouse models with targeted transporter deletions.
Main Methods:
- Review of studies utilizing genetically engineered mice with targeted disruption of dopamine transporter (DAT), serotonin transporter (SERT), and norepinephrine transporter (NET).
- Analysis of in vivo data from these animal models.
Main Results:
- Genetically deleted mouse models have provided significant insights into the functional importance of monoamine transporters.
- These models have aided in resolving issues regarding the specificity and mechanisms of action of pharmacological agents.
- Advances in understanding homeostatic control of monoaminergic transmission have been achieved.
Conclusions:
- Mice with targeted genetic deletion of DAT, SERT, and NET are invaluable tools for studying monoamine transporter function.
- These models facilitate in vivo evaluation of transporter roles in physiology, pathology, and drug development.