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Nat Commun. 2016 Feb 12;7:10702. doi: 10.1038/ncomms10702.

Loss of UBE3A from TH-expressing neurons suppresses GABA co-release and enhances VTA-NAc optical self-stimulation.

Author information

1
Curriculum in Neurobiology, University of North Carolina, Chapel Hill, 27599 North Carolina, USA.
2
Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, 27599 North Carolina, USA.
3
Neuroscience Center, University of North Carolina, Chapel Hill, 27599 North Carolina, USA.
4
Department of Psychiatry, University of North Carolina, Chapel Hill, 27599 North Carolina, USA.
5
Inscopix Inc, Palo Alto, 94303 California, USA.
6
Bowles Center for Alcohol Studies, University of North Carolina, Chapel Hill, 27599 North Carolina, USA.
7
Carolina Institute for Developmental Disabilities, University of North Carolina, Chapel Hill, 27599 North Carolina, USA.

Abstract

Motivated reward-seeking behaviours are governed by dopaminergic ventral tegmental area projections to the nucleus accumbens. In addition to dopamine, these mesoaccumbal terminals co-release other neurotransmitters including glutamate and GABA, whose roles in regulating motivated behaviours are currently being investigated. Here we demonstrate that loss of the E3-ubiquitin ligase, UBE3A, from tyrosine hydroxylase-expressing neurons impairs mesoaccumbal, non-canonical GABA co-release and enhances reward-seeking behaviour measured by optical self-stimulation.

PMID:
26869263
PMCID:
PMC4754338
DOI:
10.1038/ncomms10702
[Indexed for MEDLINE]
Free PMC Article

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