Dexamethasone enhances NT-3 expression in rat hippocampus after traumatic brain injury

Jen Tsung Yang; Tsong Hai Lee; Hsu Huei Weng; Chen Nen Chang; Wen Cheng Chen; Wan Chun Cheng; June Hsieh Wu

doi:10.1016/j.expneurol.2004.12.023

Dexamethasone enhances NT-3 expression in rat hippocampus after traumatic brain injury

Jen Tsung Yang, Tsong Hai Lee, Hsu Huei Weng, Chen Nen Chang, Wen Cheng Chen, Wan Chun Cheng, June Hsieh Wu^*

^*Corresponding author for this work

Department of Microbiology and Immunology

Research output: Contribution to journal › Journal Article › peer-review

24 Scopus citations

Abstract

The cellular events in traumatic brain injury (TBI) are complicated, and the factors mediating neurotrophins to protect and repair the injured brain cells are only beginning to be identified. This study examined the effect of dexamethasone (DEX) on neurotrophin-3 (NT-3) expression following TBI. Levels of NT-3 mRNA and protein in rat hippocampus were measured using in situ hybridization and immunohistochemistry, respectively. After TBI, the NT-3 mRNA expression was down-regulated during the first 24 h. DEX reversed the post-traumatic reduction of NT-3 mRNA expression at 2, 4, 6, and 12 h in the hippocampus, and also decreased the cell death in hippocampal hilum and supraventricular cerebral cortex after 7 days. The NT-3 protein levels generally corresponded to the mRNA levels in the hippocampal region. DEX enhanced the NT-3 expression after TBI, indicating that post-traumatic neuroprotection in the hippocampus is at least partially mediated by NT-3 and thus can be modulated by DEX treatment.

Original language	English
Pages (from-to)	437-443
Number of pages	7
Journal	Experimental Neurology
Volume	192
Issue number	2
DOIs	https://doi.org/10.1016/j.expneurol.2004.12.023
State	Published - 04 2005

Keywords

Dexamethasone
Hippocampus
Immunohistochemistry
In situ hybridization
Neurotrophin-3
Traumatic brain injury

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10.1016/j.expneurol.2004.12.023

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title = "Dexamethasone enhances NT-3 expression in rat hippocampus after traumatic brain injury",

abstract = "The cellular events in traumatic brain injury (TBI) are complicated, and the factors mediating neurotrophins to protect and repair the injured brain cells are only beginning to be identified. This study examined the effect of dexamethasone (DEX) on neurotrophin-3 (NT-3) expression following TBI. Levels of NT-3 mRNA and protein in rat hippocampus were measured using in situ hybridization and immunohistochemistry, respectively. After TBI, the NT-3 mRNA expression was down-regulated during the first 24 h. DEX reversed the post-traumatic reduction of NT-3 mRNA expression at 2, 4, 6, and 12 h in the hippocampus, and also decreased the cell death in hippocampal hilum and supraventricular cerebral cortex after 7 days. The NT-3 protein levels generally corresponded to the mRNA levels in the hippocampal region. DEX enhanced the NT-3 expression after TBI, indicating that post-traumatic neuroprotection in the hippocampus is at least partially mediated by NT-3 and thus can be modulated by DEX treatment.",

keywords = "Dexamethasone, Hippocampus, Immunohistochemistry, In situ hybridization, Neurotrophin-3, Traumatic brain injury",

author = "Yang, {Jen Tsung} and Lee, {Tsong Hai} and Weng, {Hsu Huei} and Chang, {Chen Nen} and Chen, {Wen Cheng} and Cheng, {Wan Chun} and Wu, {June Hsieh}",

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doi = "10.1016/j.expneurol.2004.12.023",

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AU - Yang, Jen Tsung

AU - Lee, Tsong Hai

AU - Weng, Hsu Huei

AU - Chang, Chen Nen

AU - Chen, Wen Cheng

AU - Cheng, Wan Chun

AU - Wu, June Hsieh

PY - 2005/4

Y1 - 2005/4

N2 - The cellular events in traumatic brain injury (TBI) are complicated, and the factors mediating neurotrophins to protect and repair the injured brain cells are only beginning to be identified. This study examined the effect of dexamethasone (DEX) on neurotrophin-3 (NT-3) expression following TBI. Levels of NT-3 mRNA and protein in rat hippocampus were measured using in situ hybridization and immunohistochemistry, respectively. After TBI, the NT-3 mRNA expression was down-regulated during the first 24 h. DEX reversed the post-traumatic reduction of NT-3 mRNA expression at 2, 4, 6, and 12 h in the hippocampus, and also decreased the cell death in hippocampal hilum and supraventricular cerebral cortex after 7 days. The NT-3 protein levels generally corresponded to the mRNA levels in the hippocampal region. DEX enhanced the NT-3 expression after TBI, indicating that post-traumatic neuroprotection in the hippocampus is at least partially mediated by NT-3 and thus can be modulated by DEX treatment.

AB - The cellular events in traumatic brain injury (TBI) are complicated, and the factors mediating neurotrophins to protect and repair the injured brain cells are only beginning to be identified. This study examined the effect of dexamethasone (DEX) on neurotrophin-3 (NT-3) expression following TBI. Levels of NT-3 mRNA and protein in rat hippocampus were measured using in situ hybridization and immunohistochemistry, respectively. After TBI, the NT-3 mRNA expression was down-regulated during the first 24 h. DEX reversed the post-traumatic reduction of NT-3 mRNA expression at 2, 4, 6, and 12 h in the hippocampus, and also decreased the cell death in hippocampal hilum and supraventricular cerebral cortex after 7 days. The NT-3 protein levels generally corresponded to the mRNA levels in the hippocampal region. DEX enhanced the NT-3 expression after TBI, indicating that post-traumatic neuroprotection in the hippocampus is at least partially mediated by NT-3 and thus can be modulated by DEX treatment.

KW - Dexamethasone

KW - Hippocampus

KW - Immunohistochemistry

KW - In situ hybridization

KW - Neurotrophin-3

KW - Traumatic brain injury

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M3 - 文章

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AN - SCOPUS:14844311317

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VL - 192

SP - 437

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JO - Experimental Neurology

JF - Experimental Neurology

IS - 2

ER -

Dexamethasone enhances NT-3 expression in rat hippocampus after traumatic brain injury

Abstract

Keywords

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