Loss of UBE3A from TH-expressing neurons suppresses GABA co-release and enhances VTA-NAc optical self-stimulation.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 26869263.
- Also identified by DOI 10.1038/ncomms10702 and PMC identifier 4754338.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- Behavior, Animal
- Dopamine
- Dopaminergic Neurons
- Motivation
- Nucleus Accumbens
- Self Stimulation
- Tyrosine 3-Monooxygenase
- Ubiquitin-Protein Ligases
- Ventral Tegmental Area
- gamma-Aminobutyric Acid