Amo Ryunosuke, Uchida Naoshige, Watabe-Uchida Mitsuko
Department of Molecular and Cellular Biology, Center for Brain Science, Harvard University, Cambridge, MA 02138, USA.
bioRxiv. 2023 Nov 9:2023.11.09.566472. doi: 10.1101/2023.11.09.566472.
Midbrain dopamine neurons are thought to signal reward prediction errors (RPEs) but the mechanisms underlying RPE computation, particularly contributions of different neurotransmitters, remain poorly understood. Here we used a genetically-encoded glutamate sensor to examine the pattern of glutamate inputs to dopamine neurons. We found that glutamate inputs exhibit virtually all of the characteristics of RPE, rather than conveying a specific component of RPE computation such as reward or expectation. Notably, while glutamate inputs were transiently inhibited by reward omission, they were excited by aversive stimuli. Opioid analgesics altered dopamine negative responses to aversive stimuli toward more positive responses, while excitatory responses of glutamate inputs remained unchanged. Our findings uncover previously unknown synaptic mechanisms underlying RPE computations; dopamine responses are shaped by both synergistic and competitive interactions between glutamatergic and GABAergic inputs to dopamine neurons depending on valences, with competitive interactions playing a role in responses to aversive stimuli.
中脑多巴胺神经元被认为用于信号奖励预测误差(RPE),但其RPE计算的潜在机制,尤其是不同神经递质的作用,仍知之甚少。在此,我们使用基因编码的谷氨酸传感器来检测多巴胺神经元的谷氨酸输入模式。我们发现,谷氨酸输入几乎呈现出RPE的所有特征,而不是传达RPE计算的特定组成部分,如奖励或预期。值得注意的是,虽然谷氨酸输入在奖励缺失时会被短暂抑制,但它们会被厌恶刺激所兴奋。阿片类镇痛药将多巴胺对厌恶刺激的负反应改变为更积极的反应,而谷氨酸输入的兴奋反应保持不变。我们的研究结果揭示了RPE计算背后以前未知的突触机制;多巴胺反应是由多巴胺神经元的谷氨酸能和γ-氨基丁酸能输入之间的协同和竞争相互作用根据效价塑造的,竞争相互作用在对厌恶刺激的反应中起作用。