从表达酪氨酸羟化酶的神经元中缺失泛素蛋白连接酶E3A会抑制GABA共同释放，并增强腹侧被盖区-伏隔核的光学自我刺激。
Loss of UBE3A from TH-expressing neurons suppresses GABA co-release and enhances VTA-NAc optical self-stimulation.
作者信息
Berrios Janet, Stamatakis Alice M, Kantak Pranish A, McElligott Zoe A, Judson Matthew C, Aita Megumi, Rougie Marie, Stuber Garret D, Philpot Benjamin D
机构信息
Curriculum in Neurobiology, University of North Carolina, Chapel Hill, 27599 North Carolina, USA.
Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, 27599 North Carolina, USA.
出版信息
Nat Commun. 2016 Feb 12;7:10702. doi: 10.1038/ncomms10702.
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.
动机性奖赏寻求行为受多巴胺能腹侧被盖区向伏隔核的投射所支配。除多巴胺外，这些中脑伏隔核终末还共同释放包括谷氨酸和γ-氨基丁酸在内的其他神经递质，目前正在研究它们在调节动机行为中的作用。在这里，我们证明，从表达酪氨酸羟化酶的神经元中缺失E3泛素连接酶UBE3A会损害中脑伏隔核非典型γ-氨基丁酸的共同释放，并增强通过光学自我刺激测量的奖赏寻求行为。
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