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Kim, Jae-Ick
Neural Circuit and Neurodegenerative Disease Lab.
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Aldehyde dehydrogenase 1a1 mediates a GABA synthesis pathway in midbrain dopaminergic neurons

Author(s)
Kim, Jae-IckGanesan, SubhashreeLuo, Sarah X.Wu, Yu-WeiPark, EstherHuang, Eric J.Chen, LuDing, Jun B.
Issued Date
2015-10
DOI
10.1126/science.aac4690
URI
https://scholarworks.unist.ac.kr/handle/201301/20943
Fulltext
http://science.sciencemag.org/content/350/6256/102
Citation
SCIENCE, v.350, no.6256, pp.102 - 106
Abstract
Midbrain dopamine neurons are an essential component of the basal ganglia circuitry, playing key roles in the control of fine movement and reward. Recently, it has been demonstrated that gamma-aminobutyric acid (GABA), the chief inhibitory neurotransmitter, is co-released by dopamine neurons. Here, we show that GABA co-release in dopamine neurons does not use the conventional GABA-synthesizing enzymes, glutamate decarboxylases GAD65 and GAD67. Our experiments reveal an evolutionarily conserved GABA synthesis pathway mediated by aldehyde dehydrogenase 1a1 (ALDH1a1). Moreover, GABA co-release is modulated by ethanol (EtOH) at concentrations seen in blood alcohol after binge drinking, and diminished ALDH1a1 leads to enhanced alcohol consumption and preference. These findings provide insights into the functional role of GABA co-release in midbrain dopamine neurons, which may be essential for reward-based behavior and addiction
Publisher
AMER ASSOC ADVANCEMENT SCIENCE
ISSN
0036-8075
Keyword
ALCOHOL-METABOLIZING GENESRETINOIC ACIDSYNAPTIC PLASTICITYPARKINSONS-DISEASEMODULATIONSTRIATUMPUTRESCINESYSTEMTRANSMISSIONPOLYAMINES

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