Retraction notice to “THE EFFECT OF MATERNAL INFECTION ON COGNITIVE DEVELOPMENT AND HIPPOCAMPUS NEURONAL APOPTOSIS, PROLIFERATION AND DIFFERENTIATION IN THE NEONATAL RATS” [Neuroscience 246 (2013) 422–434]

Jiang, Peifang; Zhu, Tao; Gao, Jing; Gao, Feng; Mao, Shishi; Zhao, Wenting; Gu, Weizhong; Yu, Huimin

doi:10.1016/j.neuroscience.2013.04.021

Cited by 6 publications

(3 citation statements)

References 47 publications

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“…The neuron-specific microtubule-associated protein 2 was used to identify neurons[5657]. Briefly, after the culture medium was discarded, the cells were fixed in cold 4% paraformaldehyde for 30 minutes, treated with 0.3% Triton X-100 for 20 minutes, and then incubated with 30 μL of 0.3% H 2 O 2 /methanol solution at room temperature for 10 minutes, 30 μL of normal goat serum at room temperature for 10 minutes, 50 μL of mouse anti-microtubule-associated protein 2 polyclonal antibody (1:1,000; Chemicon) at 4°C overnight, and FITC-labeled sheep anti-mouse IgG (1:100; Chemicon) at 37°C for 1 hour.…”

Section: Methodsmentioning

confidence: 99%

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Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

Guo

et al. 2014

Neural Regen Res

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The microglia-mediated inflammatory reaction promotes neuronal damage under cerebral ischemia/hypoxia conditions. We therefore speculated that inhibition of hypoxia-induced microglial activation may alleviate neuronal damage. To test this hypothesis, we co-cultured ginsenoside Rb1, an active component of ginseng, and cortical neurons. Ginsenoside Rb1 protected neuronal morphology and structure in a single hypoxic culture system and in a hypoxic co-culture system with microglia, and reduced neuronal apoptosis and caspase-3 production. The protective effect was observable prior to placing in co-culture. Additionally, ginsenoside Rb1 inhibited levels of tumor necrosis factor-α in a co-culture system containing activated N9 microglial cells. Ginsenoside Rb1 also significantly decreased nitric oxide and superoxide production induced by N9 microglia. Our findings indicate that ginsenoside Rb1 attenuates damage to cerebral cortex neurons by downregulation of nitric oxide, superoxide, and tumor necrosis factor-α expression in hypoxia-activated microglia.

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Section: Methodsmentioning

confidence: 99%

“…Between the incubation steps, cells were rinsed with PBS. Finally, the slices were mounted with phosphoglycerol[545556] and observed with fluorescence microscopy. The negative control was incubated with 0.01 mol/L PBS instead of primary antibody.…”

Section: Methodsmentioning

confidence: 99%

Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

Guo

et al. 2014

Neural Regen Res

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“…Chronic antibiotic treatment led to a decrease in CRH receptor mRNA levels in the brains of rats ( 361 ). The introduction of pathogenic bacteria reduced cognitive abilities and heightened anxiety-like behaviors ( 362 , 363 ). Exposure of neonatal animals to low-dose endotoxins resulted in the activation of TLRs ( 364 , 365 ).…”

Section: The Relationship Between the Microbiota Hpa Axis And Cognitionmentioning

confidence: 99%

Signalling cognition: the gut microbiota and hypothalamic-pituitary-adrenal axis

2023

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Cognitive function in humans depends on the complex and interplay between multiple body systems, including the hypothalamic-pituitary-adrenal (HPA) axis. The gut microbiota, which vastly outnumbers human cells and has a genetic potential that exceeds that of the human genome, plays a crucial role in this interplay. The microbiota-gut-brain (MGB) axis is a bidirectional signalling pathway that operates through neural, endocrine, immune, and metabolic pathways. One of the major neuroendocrine systems responding to stress is the HPA axis which produces glucocorticoids such as cortisol in humans and corticosterone in rodents. Appropriate concentrations of cortisol are essential for normal neurodevelopment and function, as well as cognitive processes such as learning and memory, and studies have shown that microbes modulate the HPA axis throughout life. Stress can significantly impact the MGB axis via the HPA axis and other pathways. Animal research has advanced our understanding of these mechanisms and pathways, leading to a paradigm shift in conceptual thinking about the influence of the microbiota on human health and disease. Preclinical and human trials are currently underway to determine how these animal models translate to humans. In this review article, we summarize the current knowledge of the relationship between the gut microbiota, HPA axis, and cognition, and provide an overview of the main findings and conclusions in this broad field.

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Microbiota-Gut-Brain Axis and Cognitive Function

Gareau

2014

Advances in Experimental Medicine and Biology

141

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Recent studies have demonstrated a clear association between changes in the microbiota and cognitive behavior. Intestinal dysbiosis, as modeled using GF mice (containing no microbiota), bacterial infection with an enteric pathogen, and administration of probiotics, can modulate cognitive behavior including learning and memory. This chapter will highlight recent findings in both human and animal studies indicating how changes in the composition and diversity of the microbiota can impact behavior and brain physiology in both disease states and in health. Cognitive behavior can not only be affected in cases of intestinal disease, but also manifests changes in extra-intestinal disease conditions.

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Retraction notice to “THE EFFECT OF MATERNAL INFECTION ON COGNITIVE DEVELOPMENT AND HIPPOCAMPUS NEURONAL APOPTOSIS, PROLIFERATION AND DIFFERENTIATION IN THE NEONATAL RATS” [Neuroscience 246 (2013) 422–434]

Cited by 6 publications

References 47 publications

Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

Signalling cognition: the gut microbiota and hypothalamic-pituitary-adrenal axis

Microbiota-Gut-Brain Axis and Cognitive Function

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