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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Behavior, Animal*
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Dopamine / metabolism*
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Dopaminergic Neurons / metabolism*
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Immunohistochemistry
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In Situ Hybridization, Fluorescence
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Motivation / genetics*
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Neural Pathways
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Neurons / metabolism
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Nucleus Accumbens / metabolism*
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Optogenetics
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Patch-Clamp Techniques
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Reinforcement, Psychology
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Reward
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Self Stimulation*
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Stereotaxic Techniques
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Synaptic Transmission / genetics
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Tyrosine 3-Monooxygenase / metabolism*
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Ubiquitin-Protein Ligases / genetics*
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Ventral Tegmental Area / cytology
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Ventral Tegmental Area / metabolism*
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gamma-Aminobutyric Acid / metabolism*
Substances
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gamma-Aminobutyric Acid
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Tyrosine 3-Monooxygenase
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Ube3a protein, mouse
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Ubiquitin-Protein Ligases
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Dopamine