@article {69692,
	title = {Elevated IL-22 as a result of stress-induced gut leakage suppresses septal neuron activation to ameliorate anxiety-like behavior.},
	journal = {Immunity},
	year = {2024},
	month = {2024 Dec 04},
	pages = {S1074-7613(24)00523-5},
	abstract = {<p>Psychological stress and its sequelae pose a major challenge to public health. Immune activation is conventionally thought to aggravate stress-related mental diseases such as anxiety disorders and depression. Here, we sought to identify potentially beneficial consequences of immune activation in response to stress. We showed that stress led to increased interleukin (IL)-22 production in the intestine as a result of stress-induced gut leakage. IL-22 was both necessary and sufficient to attenuate stress-induced anxiety behaviors in mice. More specifically, IL-22 gained access to the septal area of the brain and directly suppressed neuron activation. Furthermore, human patients with clinical depression displayed reduced IL-22 levels, and exogenous IL-22 treatment ameliorated depressive-like behavior elicited by chronic stress in mice. Our study thus identifies a gut-brain axis in response to stress, whereby IL-22 reduces neuronal activation and concomitant anxiety behavior, suggesting that early immune activation can provide protection against psychological stress.</p>
},
	issn = {1097-4180},
	doi = {10.1016/j.immuni.2024.11.008},
	author = {Xia, Mengyu and Lu, Junmei and Lan, Jiabin and Teng, Teng and Shiao, Rani and Sun, Hongbin and Jin, Zheyu and Liu, Xueer and Wang, Jie and Wu, Hongyan and Wang, Changchun and Yi, Han and Qi, Qingqing and Li, Jixi and Schneeberger, Marc and Shen, Wei and Lu, Boxun and Chen, Lei and Ilanges, Anoj and Zhou, Xinyu and Yu, Xiaofei}
}
@article {65107,
	title = {A neuronal pathway that commands deceleration in Drosophila larval light-avoidance.},
	journal = {Neuroscience Bulletin},
	volume = {35},
	year = {2019},
	month = {2019 Dec 1},
	abstract = {<p>When facing a sudden danger or aversive condition while engaged in on-going forward motion, animals transiently slow down and make a turn to escape. The neural mechanisms underlying stimulation-induced deceleration in avoidance behavior are largely unknown. Here, we report that in Drosophila larvae, light-induced deceleration was commanded by a continuous neural pathway that included prothoracicotropic hormone neurons, eclosion hormone neurons, and tyrosine decarboxylase 2 motor neurons (the PET pathway). Inhibiting neurons in the PET pathway led to defects in light-avoidance due to insufficient deceleration and head casting. On the other hand, activation of PET pathway neurons specifically caused immediate deceleration in larval locomotion. Our findings reveal a neural substrate for the emergent deceleration response and provide a new understanding of the relationship between behavioral modules in animal avoidance responses.</p>
},
	issn = {1995-8218},
	doi = {10.1007/s12264-019-00349-w},
	author = {Gong, Caixia and Ouyang, Zhenhuan and Zhao, Weiqiao and Wang, Jie and Li, Kun and Zhou, Peipei and Zhao, Ting and Zheng, Nenggan and Gong, Zhefeng}
}
