OBJECTIVE Our aim was to explore the effect of γ-aminobutyric acid (GABA) signaling in the nucleus accumbens (NAc) on promoting gastric function and food intake through glucagon-like peptide 1 (GLP-1)-sensitive gastric distension (GD) neurons under the regulatory control of the zona incerta (ZI). METHODS GABA neuronal projections were traced using retrograde tracing following fluorescence immunohistochemistry. An extracellular electrophysiological recording method was used to observe the firing of neurons in the NAc. HPLC was used to quantify the GABA and glutamate levels in the NAc after electrical stimulation of the ZI. Gastric functions including gastric motility and secretion, as well as food intake, were measured after the administration of different concentrations of GABA in the NAc or electrical stimulation of the ZI. RESULTS Some of the GABA-positive neurons arising from the ZI projected to the NAc. Some GABA-A receptor (GABA-AR)-immunoreactive neurons in the NAc were also positive for GLP-1 receptor (GLP-1R) immunoreactivity. The firing of most GLP-1-sensitive GD neurons was decreased by GABA infusion in the NAc. Intra-NAc GABA administration also promoted gastric function and food intake. The responses induced by GABA were partially blocked by the GABA-AR antagonist bicuculline (BIC) and weakened by the GLP-1R antagonist exendin 9-39 (Ex9). Electrical stimulation of the ZI changed the firing patterns of most GLP-1-sensitive GD neurons in the NAc and promoted gastric function and food intake. Furthermore, these excitatory effects induced by electrical stimulation of the ZI were weakened by preadministration of BIC in the NAc. CONCLUSION Retrograde tracing and immunohistochemical staining showed a GABAergic pathway from the ZI to the NAc. GABAergic and GLP-1 mechanisms in the NAc are involved in the control of gastric function and food intake. In addition, the interaction (direct or indirect) between the ZI and these NAc mechanisms is involved in the control of gastric function and food intake.

中文翻译：

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伏核中的不定带投射神经元和 GABA 能和 GLP-1 机制参与控制胃功能和食物摄入

目的 我们的目的是探讨伏隔核 (NAc) 中的 γ-氨基丁酸 (GABA) 信号对通过胰高血糖素样肽 1 (GLP-1) 敏感的胃扩张 (GD) 神经元促进胃功能和食物摄入的影响在 zona incerta (ZI) 的监管控制下。方法在荧光免疫组织化学之后使用逆行追踪追踪 GABA 神经元投射。使用细胞外电生理记录方法观察 NAc 中神经元的放电。在 ZI 电刺激后，使用 HPLC 来量化 NAc 中的 GABA 和谷氨酸水平。在 NAc 中施用不同浓度的 GABA 或 ZI 的电刺激后，测量胃功能，包括胃动力和分泌，以及食物摄入量。结果 一些由 ZI 产生的 GABA 阳性神经元投射到 NAc。NAc 中的一些 GABA-A 受体 (GABA-AR) 免疫反应神经元也对 GLP-1 受体 (GLP-1R) 免疫反应呈阳性。大多数 GLP-1 敏感 GD 神经元的放电因 NAc 中的 GABA 输注而降低。NAc GABA 内给药也促进胃功能和食物摄入。GABA 诱导的反应被 GABA-AR 拮抗剂荷包牡丹碱 (BIC) 部分阻断，并被 GLP-1R 拮抗剂毒蜥外泌肽 9-39 (Ex9) 减弱。ZI 的电刺激改变了 NAc 中大多数 GLP-1 敏感的 GD 神经元的放电模式，并促进了胃功能和食物摄入。此外，这些由 ZI 电刺激引起的兴奋作用因在 NAc 中预先施用 BIC 而减弱。结论逆行示踪和免疫组织化学染色显示从 ZI 到 NAc 的 GABA 途径。NAc 中的 GABA 能和 GLP-1 机制参与控制胃功能和食物摄入。此外，ZI 和这些 NAc 机制之间的相互作用（直接或间接）涉及胃功能和食物摄入的控制。