AMPK activation prevents prenatal stress-induced cognitive impairment: Modulation of mitochondrial content and oxidative stress

Cao, Ke; Zheng, Adi; Xu, Jie; Li, Hao; Liu, Jing; Peng, Yunhua; Long, Jiangang; Zou, Xuan; Li, Yuan; Chen, Cong; Liu, Jiankang; Feng, Zhihui

doi:10.1016/j.freeradbiomed.2014.07.029

Cited by 51 publications

(38 citation statements)

References 41 publications

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“…Herein, we report a suppression of chaperoning/stress response proteins in the adult hippocampus at age 6 months from identically exposed animals that was coupled to an increase in one form of superoxide dismutase and an impact on the NRF2 mediated oxidative stress response pathway. Similar findings of sustained oxidative stress were noted in offspring experiencing restraint stress during pregnancy [82], [83, 84], prenatal hypoxia [85, 86], heavy metal exposure [87, 88], and malnutrition [89–91]. Though a trend toward impaired GSH/GSSG ratio and antioxidant enzyme activities within the hippocampus of adult offspring with prior CSE was evident, the cerebral cortex of offspring with prior CSE did exhibit a loss of total glutathione.…”

Section: Discussionsupporting

confidence: 71%

Developmental cigarette smoke exposure II: Hippocampus proteome and metabolome profiles in adult offspring

Neal

Jagadapillai

Chen

et al. 2016

Reproductive Toxicology

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Exposure to cigarette smoke during development is linked to neurodevelopmental delays and cognitive impairment including impulsivity, attention deficit disorder, and lower IQ. Utilizing a murine experimental model of "active" inhalation exposure to cigarette smoke spanning the entirety of gestation and through human third trimester equivalent hippocampal development [gestation day 1 (GD1) through postnatal day 21 (PD21)], we examined hippocampus proteome and metabolome alterations present at a time during which developmental cigarette smoke exposure (CSE)-induced behavioral and cognitive impairments are evident in adult animals from this model system. At six month of age, carbohydrate metabolism and lipid content in the hippocampus of adult offspring remained impacted by prior exposure to cigarette smoke during the critical period of hippocampal ontogenesis indicating limited glycolysis. These findings indicate developmental CSE-induced systemic glucose availability may limit both organism growth and developmental trajectory, including the capacity for learning and memory.

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Section: Discussionsupporting

confidence: 71%

Developmental cigarette smoke exposure II: Hippocampus proteome and metabolome profiles in adult offspring

Neal

Jagadapillai

Chen

et al. 2016

Reproductive Toxicology

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“…Hippocampal AMPK signaling can also suppress and delay the appearance of Alzheimer's disease pathology and prevent cognitive dysfunction induced by different modulators such as stress and streptozotocin [32,33]. Previous studies have demonstrated that during the early phase of Alzheimer's disease, patients begin to decrease food intake, which may be associated with decreased AMPK signaling [34].…”

Section: Discussionmentioning

confidence: 99%

“…The β-amyloid (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) and β-amyloid were dissolved in sterile saline and stored at −20°C before use. The infusion of β-amyloid (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) into the LV causes the accumulation of β-amyloid whereas the infusion of β-amyloid , the reverse sequence of β-amyloid (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), does not accumulate in the brain, as confirmed by immunohistochemistry using β-amyloid antibody [4,21].…”

Section: Animal Care and Surgical Proceduresmentioning

confidence: 99%

“…The infusion of β-amyloid (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) into the LV causes the accumulation of β-amyloid whereas the infusion of β-amyloid , the reverse sequence of β-amyloid (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), does not accumulate in the brain, as confirmed by immunohistochemistry using β-amyloid antibody [4,21]. Each β-amyloid solution was infused via an osmotic pump (Alzet Osmotic Pump Company, Cupertino, CA) at the rate of 16.8 nmol/day for 3 days.…”

Section: Animal Care and Surgical Proceduresmentioning

confidence: 99%

“…Each β-amyloid solution was infused via an osmotic pump (Alzet Osmotic Pump Company, Cupertino, CA) at the rate of 16.8 nmol/day for 3 days. The cannula was secured with dental cement and connected to 22-gauge tubing filled with one of the following: β-amyloid (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), designated AD; β-amyloid (35-25) designated Non-AD (negative control).…”

Section: Animal Care and Surgical Proceduresmentioning

confidence: 99%

See 2 more Smart Citations

Central acylated ghrelin improves memory function and hippocampal AMPK activation and partly reverses the impairment of energy and glucose metabolism in rats infused with β-amyloid

et al. 2015

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The effects of forced exercise and zinc supplementation during pregnancy on prenatally stress‐induced behavioral and neurobiological consequences in adolescent female rat offspring

Sameei

Fatehfar

Abdollahzadeh

et al. 2023

Developmental Psychobiology

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Prenatal manipulations can lead to neurobehavioral changes in the offspring. In this study, individual and combined effects of forced exercise and zinc supplementation during pregnancy on prenatally restraint stress (PRS)‐induced behavioral impairments, neuro‐inflammatory responses, and oxidative stress have been investigated in adolescent female rat offspring. Pregnant rats were divided into five groups: control; restraint stress (RS); RS + exercise stress (RS + ES), RS + zinc supplementation (RS + Zn); and RS + ES + Zn. All the pregnant rats (except control) were exposed to RS from gestational days 15 to 19. Pregnant rats in ES groups were subjected to forced treadmill exercise (30 min/daily), and in Zn groups to zinc sulfate (30 mg/kg/orally), throughout the pregnancy. At postnatal days 25–27, anxiety‐like and stress‐coping behaviors were recorded, and the gene expressions of interleukin‐1β (IL‐1β) and tumor necrosis factor‐α (TNF‐α) and the concentration of total antioxidant capacity were measured in the prefrontal cortex. PRS significantly enhanced anxiety, generated passive coping behaviors, increased IL‐1β and TNF‐α expression, and decreased the antioxidant capacity. ES potentiated while zinc reversed PRS‐induced behavioral impairments. Prenatal zinc also restored the anti‐inflammatory and antioxidant capacity but had no effect on additive responses imposed by the combination of RS and ES. Suppression of PRS‐induced behavioral and neurobiological impairments by zinc suggests the probable clinical importance of zinc on PRS‐induced changes on child temperament.

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AMPK activation prevents prenatal stress-induced cognitive impairment: Modulation of mitochondrial content and oxidative stress

Cited by 51 publications

References 41 publications

Developmental cigarette smoke exposure II: Hippocampus proteome and metabolome profiles in adult offspring

Developmental cigarette smoke exposure II: Hippocampus proteome and metabolome profiles in adult offspring

Central acylated ghrelin improves memory function and hippocampal AMPK activation and partly reverses the impairment of energy and glucose metabolism in rats infused with β-amyloid

The effects of forced exercise and zinc supplementation during pregnancy on prenatally stress‐induced behavioral and neurobiological consequences in adolescent female rat offspring

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