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Spatial and temporal correlation in progressive degeneration of neurons and astrocytes in contusion-induced spinal cord injury

Authors
Min, KJ; Jeong, HK; Kim, B; Hwang, DH; Shin, HY; Nguyen, AT; Kim, JH; Jou, I; Kim, BG; Joe, EH
Citation
Journal of neuroinflammation, 9:100-100, 2012
Journal Title
Journal of neuroinflammation
ISSN
1742-2094
Abstract
BACKGROUND: Traumatic spinal cord injury (SCI) causes acute neuronal death followed by delayed secondary neuronal damage. However, little is known about how microenvironment regulating cells such as microglia, astrocytes, and blood inflammatory cells behave in early SCI states and how they contribute to delayed neuronal death.



METHODS: We analyzed the behavior of neurons and microenvironment regulating cells using a contusion-induced SCI model, examining early (3-6 h) to late times (14 d) after the injury.



RESULTS: At the penumbra region close to the damaged core (P1) neurons and astrocytes underwent death in a similar spatial and temporal pattern: both neurons and astrocytes died in the medial and ventral regions of the gray matter between 12 to 24 h after SCI. Furthermore, mRNA and protein levels of transporters of glutamate (GLT-1) and potassium (Kir4.1), functional markers of astrocytes, decreased at about the times that delayed neuronal death occurred. However, at P1 region, ramified Iba-1+ resident microglia died earlier (3 to 6 h) than neurons (12 to 24 h), and at the penumbra region farther from the damaged core (P2), neurons were healthy where microglia were morphologically activated. In addition, round Iba-1/CD45-double positive monocyte-like cells appeared after neurons had died, and expressed phagocytic markers, including mannose receptors, but rarely expressed proinflammatory mediators.



CONCLUSION: Loss of astrocyte function may be more critical for delayed neuronal death than microglial activation and monocyte infiltration.
MeSH terms
AnimalsAstrocytes/metabolism/*pathologyCalcium-Binding Proteins/biosynthesisContusions/metabolism/*pathology*Disease ProgressionFemaleMicrofilament Proteins/biosynthesisNerve Degeneration/metabolism/*pathologyNeurons/metabolism/*pathologyRatsRats, Sprague-DawleySpinal Cord Injuries/metabolism/*pathologyTime Factors
DOI
10.1186/1742-2094-9-100
PMID
22632146
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
Journal Papers > School of Medicine / Graduate School of Medicine > Brain Science
AJOU Authors
김, 범수황, 동훈주, 일로김, 병곤조, 은혜
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