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Effect of Heat Stress on Hippocampal Neurogenesis: Insights into the Cellular and Molecular Basis of Neuroinflammation-Induced Deficits

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Abstract

Heat stress is known to result in neuroinflammation, neuronal damage, and disabilities in learning and memory in animals and humans. It has previously been reported that cognitive impairment caused by neuroinflammation may at least in part be mediated by defective hippocampal neurogenesis, and defective neurogenesis has been linked to aberrantly activated microglial cells. Moreover, the release of cytokines within the brain has been shown to contribute to the disruption of cognitive functions in several conditions following neuroinflammation. In this review, we summarize evolving evidence for the current understanding of inflammation-induced deficits in hippocampal neurogenesis, and the resulting behavioral impairments after heat stress. Furthermore, we provide valuable insights into the molecular and cellular mechanisms underlying neuroinflammation-induced deficits in hippocampal neurogenesis, particularly relating to cognitive dysfunction following heat stress. Lastly, we aim to identify potential mechanisms through which neuroinflammation induces cognitive dysfunction, and elucidate how neuroinflammation contributes to defective hippocampal neurogenesis. This review may therefore help to better understand the relationship between hippocampal neurogenesis and heat stress.

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Abbreviations

BDNF:

Brain-derived neurotrophic factor

BrdU:

Neurons and bromodeoxyuridine

CAT:

Catalase

CNS:

Central nervous system

COX-2:

Cyclooxygenase-2

DCX:

Doublecortin

DG:

Dentate gyrus

GCL:

Granule cell layer

GFAP:

Glial fibrillary acidic protein

GPX:

Glutathione peroxidase

GSAI-B4:

Griffonia simplicifolia lectin

GSH:

Glutathione

GSSG:

Glutathione disulfide

Iba-1:

Ionized calcium-binding adapter molecule 1

IFNγ:

Interferon-γ

IL-1β:

Interleukin-1β

IL-1R1:

Type 1 IL-1 receptor

iNOS:

Nitric oxide synthase

LPS:

Lipopolysaccharide

LTD:

Long-term depression

LTP:

Long-term potentiation

MDA:

Oxidative stress marker

miRNA:

MicroRNA

NeuN:

Neuronal nuclei

NF-κB:

Nuclear factor kappa B

NGF:

Nerve growth factor

NO:

Nitric oxide

NPC:

Neural progenitor cell

NSCs:

Neural stem cells

ROS:

Reactive oxygen species

SGZ:

Subgranular zone

SOD:

Superoxide dismutase

SVZ:

Subventricular zone

TLR-2:

Toll-like receptor 2

TNF-α:

Tumor necrosis factor α

TNF-R1:

TNF-α type 1 receptor

tPA:

Tissue-type plasminogen activator

TrkB:

Tropomyosin receptor kinase B

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Funding

This work was financially supported by the Technological Innovation Guidance Project of Shaanxi Province (No. 2020QFY10-04), National Key Research and Development Program of China (No. 2018YFE0127000), and General Project of Basic Research of Shaanxi Province (No. 2020JM-603).

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The manuscript was written through contributions of all authors. All authors have given approval to the final version of the manuscript. Review design: XZ and XC; writing—original draft preparation: XZ, JH, and YW; revised the figure and table: JH and YW; writing—review and editing: XZ, SZ, and XC.

Corresponding authors

Correspondence to Xiaoyan Zhu or Xuejun Chai.

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The authors declare that they have no conflict of interest.

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Zhu, X., Huang, J., Wu, Y. et al. Effect of Heat Stress on Hippocampal Neurogenesis: Insights into the Cellular and Molecular Basis of Neuroinflammation-Induced Deficits. Cell Mol Neurobiol 43, 1–13 (2023). https://doi.org/10.1007/s10571-021-01165-5

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  • DOI: https://doi.org/10.1007/s10571-021-01165-5

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