Acute Fasting Does Not Induce Cognitive Impairment in Mice

Preoperative baseline cognitive impairment is associated with postoperative neurocognitive disorder (PND). Fasting, and more generally, calorie restriction has been shown to exert controversial effects in clinical settings and various animal models of neurological disorders. Every patient needs acut...

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Main Authors: Hua Zheng, Hoai Ton, Lei Yang, Ning Liufu, Yuanlin Dong, Yiying Zhang, Zhongcong Xie
Format: Article
Language:English
Published: Frontiers Media S.A. 2019-08-01
Series:Frontiers in Neuroscience
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fnins.2019.00896/full
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language English
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author Hua Zheng
Hua Zheng
Hoai Ton
Lei Yang
Lei Yang
Ning Liufu
Ning Liufu
Yuanlin Dong
Yiying Zhang
Zhongcong Xie
spellingShingle Hua Zheng
Hua Zheng
Hoai Ton
Lei Yang
Lei Yang
Ning Liufu
Ning Liufu
Yuanlin Dong
Yiying Zhang
Zhongcong Xie
Acute Fasting Does Not Induce Cognitive Impairment in Mice
Frontiers in Neuroscience
acute fasting
cognitive impairment
neural activation
cellular apoptosis
mice
author_facet Hua Zheng
Hua Zheng
Hoai Ton
Lei Yang
Lei Yang
Ning Liufu
Ning Liufu
Yuanlin Dong
Yiying Zhang
Zhongcong Xie
author_sort Hua Zheng
title Acute Fasting Does Not Induce Cognitive Impairment in Mice
title_short Acute Fasting Does Not Induce Cognitive Impairment in Mice
title_full Acute Fasting Does Not Induce Cognitive Impairment in Mice
title_fullStr Acute Fasting Does Not Induce Cognitive Impairment in Mice
title_full_unstemmed Acute Fasting Does Not Induce Cognitive Impairment in Mice
title_sort acute fasting does not induce cognitive impairment in mice
publisher Frontiers Media S.A.
series Frontiers in Neuroscience
issn 1662-453X
publishDate 2019-08-01
description Preoperative baseline cognitive impairment is associated with postoperative neurocognitive disorder (PND). Fasting, and more generally, calorie restriction has been shown to exert controversial effects in clinical settings and various animal models of neurological disorders. Every patient needs acute fasting before anesthesia and surgery. However, the impact of acute fasting on cognitive function remain largely unknown. We, therefore, set out to determine whether acute fasting can induce neurotoxicity and neurobehavioral deficits in rodents. In the present system establishment study, a mouse model of acute fasting was established. The effects of the acute fasting on natural and learned behavior were evaluated in the buried food test, open field test and the Y maze test. The expression of c-Fos, the marker of neuronal activation, and caspase-3 activation, the marker of cellular apoptosis, were measured with immunohistochemistry. We found that the 9 h acute fasting increased the latency to eat food in the buried food test. The acute fasting also selectively increased the total distance and decreased the freezing time in open field test, and increased the duration in the novel arm in the Y maze test. Besides, the immunohistochemical study showed that the fasting significantly increased the c-Fos level in the hippocampus and various sub-cortical areas, including paraventricular thalamus (PVT), dorsomedial hypothalamus (DMH), lateral hypothalamus (LH), and basal amygdala (BMA). However, the acute fasting did not induce apoptosis, demonstrating by no appearance of caspase-3 activation in the corresponding brain areas. These data showed that acute fasting did not cause cellular apoptosis and cognitive impairment in the mice. Instead, the acute fasting increased the neuronal activity, enhanced the ambulatory activity and improved the spatial recognition memory in the mice. These findings will promote more research in the established system to further determine the effects of perioperative factors on the postoperative neurocognitive function and the underlying mechanisms.
topic acute fasting
cognitive impairment
neural activation
cellular apoptosis
mice
url https://www.frontiersin.org/article/10.3389/fnins.2019.00896/full
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spelling doaj-d2d39cc5183945a2b3290ef1b7e270e32020-11-24T21:44:13ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2019-08-011310.3389/fnins.2019.00896469916Acute Fasting Does Not Induce Cognitive Impairment in MiceHua Zheng0Hua Zheng1Hoai Ton2Lei Yang3Lei Yang4Ning Liufu5Ning Liufu6Yuanlin Dong7Yiying Zhang8Zhongcong Xie9Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaGeriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United StatesGeriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United StatesGeriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United StatesDepartment of Anesthesiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, ChinaGeriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United StatesDepartment of Anesthesiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaGeriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United StatesGeriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United StatesGeriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United StatesPreoperative baseline cognitive impairment is associated with postoperative neurocognitive disorder (PND). Fasting, and more generally, calorie restriction has been shown to exert controversial effects in clinical settings and various animal models of neurological disorders. Every patient needs acute fasting before anesthesia and surgery. However, the impact of acute fasting on cognitive function remain largely unknown. We, therefore, set out to determine whether acute fasting can induce neurotoxicity and neurobehavioral deficits in rodents. In the present system establishment study, a mouse model of acute fasting was established. The effects of the acute fasting on natural and learned behavior were evaluated in the buried food test, open field test and the Y maze test. The expression of c-Fos, the marker of neuronal activation, and caspase-3 activation, the marker of cellular apoptosis, were measured with immunohistochemistry. We found that the 9 h acute fasting increased the latency to eat food in the buried food test. The acute fasting also selectively increased the total distance and decreased the freezing time in open field test, and increased the duration in the novel arm in the Y maze test. Besides, the immunohistochemical study showed that the fasting significantly increased the c-Fos level in the hippocampus and various sub-cortical areas, including paraventricular thalamus (PVT), dorsomedial hypothalamus (DMH), lateral hypothalamus (LH), and basal amygdala (BMA). However, the acute fasting did not induce apoptosis, demonstrating by no appearance of caspase-3 activation in the corresponding brain areas. These data showed that acute fasting did not cause cellular apoptosis and cognitive impairment in the mice. Instead, the acute fasting increased the neuronal activity, enhanced the ambulatory activity and improved the spatial recognition memory in the mice. These findings will promote more research in the established system to further determine the effects of perioperative factors on the postoperative neurocognitive function and the underlying mechanisms.https://www.frontiersin.org/article/10.3389/fnins.2019.00896/fullacute fastingcognitive impairmentneural activationcellular apoptosismice