Orogenic belts have been among the most important locations to investigate the growth of continental crust (CC). The Eastern Kunlun Orogenic Belt (EKOB), which contains widespread Permian-Triassic granitoids, is volumetrically comparable to the Cenozoic Gangdese magmatic belt in the Tibetan Plateau and is an ideal region to investigate the mechanism of the Paleozoic-Mesozoic CC growth in this region. The Gouli batholith at the eastern end of the EKOB consists of the synchronous Xiangride granodiorite, Asiha quartz diorite (ca. 242 Ma) and adamellite. The granodiorite and quartz diorite, both of which contain magmatic enclaves, show medium-high K, calc-alkalic and metaluminous signatures and have similar rare earth element and trace element patterns to those of bulk CC. Besides, the Xiangride granodiorite displays distinct adakitic signatures (average Sr/Y of 47). The Sr-Nd isotopic values for the different types of rocks are roughly similar ((87 Sr/ 86 Sr) i = 0.708167-0.713553, ε Nd (t) =-6.8 to-5.3), while Hf isotopes are distinguishable, with ε Hf (t) granodiorite = 0.3 to 5.1 and ε Hf (t) diorite =-1.6 to 0.7. These geochemical and petrographic signatures suggest that the granodiorite originated from the partial melting of subducting oceanic crust and terrigenous sediments, and the quartz diorite and enclaves formed via the mixing of slab-derived magma and enriched mantle-derived melt. Further comprehensive analyses of the spatial and temporal distribution of regional magmatic rocks, metamorphism and sedimentary facies reveal that the Gouli batholith and most of the Permian-Triassic granitoids in the EKOB formed during the subduction of the Paleo-Tethys Ocean instead of subsequent syn-collision setting. Thus, we contend that the Permian-Triassic CC growth of the EKOB occurred in a slab

Hypothalamus-pituitary-adrenal (HPA) hyperactivity is observed in many patients suffering from depression and the mechanism underling the dysfunction of HPA axis is not well understood. Chronic stress has a causal relationship with the hyperactivity of HPA axis. Stress induces the over-synthesis of glucocorticoids, which will arrive at all the body containing the brain. It is still complicated whether glucocorticoids account for chronic stress-induced HPA axis hyperactivity and in which part of the brain the glucocorticoids account for chronic stress-induced HPA axis hyperactivity. Here, we demonstrated that glucocorticoids were indispensable and sufficient for chronic stress-induced hyperactivity of HPA axis. Although acute glucocorticoids elevation in the hippocampus and hypothalamus exerted a negative regulation of HPA axis, we found that chronic glucocorticoids elevation in the hippocampus but not in the hypothalamus accounted for chronic stress-induced hyperactivity of HPA axis. Chronic glucocorticoids exposure in the hypothalamus still exerted a negative regulation of HPA axis activity. More importantly, we found mineralocorticoid receptor (MR) - neuronal nitric oxide synthesis enzyme (nNOS) - nitric oxide (NO) pathway mediated the different roles of glucocorticoids in the hippocampus and hypothalamus in regulating HPA axis activity. This study suggests that the glucocorticoids in the hippocampus play an important role in the development of HPA axis hyperactivity and the glucocorticoids in the hypothalamus can't induce hyperactivity of HPA axis, revealing new insights into understanding the mechanism of depression.

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