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Complex network theory proposes a structural network model that abstracts the elements in a complex system into nodes and the relationship between elements into ties, which proved to be a scientific method to study the structural system of complexities. This article aims to apply the complex network theory to interpret the organization of landscape spatial structure and propose a spatial structure network construction and quantitative analysis method suitable for landscape space. The following two questions are addressed in this research: (1) How to extract the structural elements from the landscape space and realize the construction of the structural network model based on the 3D spatial information? (2) How to quantitatively analyze the organization characteristics of a spatial structure according to the particularity of landscape space? The research content of this article includes the following five aspects, which are 3D spatial information acquisition, structural element extraction, structural element description, structural network model diagramming, and quantitative index selection. Taking Nanjing Lovers Park as an example, the feasibility of this method is verified. The results show that the method proposed can guarantee the accuracy of the landscape spatial structure model, visualize the attributes of structural elements, and achieve a refined analysis of the structure organization.

Depressive symptoms, such as anhedonia, decreased social interaction, and lack of motivation, implicate brain reward systems in the pathophysiology of depression. Exposure to chronic stress impairs the function of brain reward circuits and is well-known to be involved in the etiology of depression. A transcriptomic analysis found that stress alters the expression of Rasd2in mice prefrontal cortex (PFC). Similarly, in our previous study, acute fasting decreased Rasd2expression in mice PFC, and RASD2 modulated dopamine D2 receptor (DRD2)-mediated antidepressant-like effects in ovariectomized mice. This research suggests the role of RASD2 in stress-induced depression and its underlying neural mechanisms that require further investigation. Here, we show that 5-day unpredictable mild stress (5-d UMS) exposure reduces RASD2 expression in both the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) of mice, while overexpression (but not knock-down) of Rasd2in the NAc core (NAcc) alleviates 5-d UMS-induced depression-like behaviors and activates the DRD2-cAMP-PKA-DARPP-32 signaling pathway. Further studies investigated neuronal projections between the mPFC (Cg1, PrL, and IL) and NAcc, labeled by the retrograde tracer Fluorogold. Depression-like behaviors induced by 5-d UMS were only related to inhibition of the PrL-NAcc circuit. DREADD (Designer receptors exclusively activated by designer drug) analysis found that the activation of PrL-NAcc glutaminergic projection alleviated depression-like behaviors and increased DRD2- and RASD2-positive neurons in the NAcc. Using Drd2-cretransgenic mice, we constructed mice with Rasd2overexpression in DRD2PrL-NAccneurons, finding that Rasd2overexpression ameliorated 5-d UMS-induced depression-like behaviors. These findings demonstrate a critical role for RASD2 modulation of DRD2PrL-NAccneurons in 5-d UMS-induced depression-like behaviors. In addition, the study identifies a new potential strategy for precision medical treatment of depression.