## Abstract After target ablation by olfactory bulbectomy (OBX), the murine olfactory epithelium (OE) undergoes degenerative changes leading to apoptosis of olfactory receptor neurons (ORNs) followed by regenerative changes that include proliferation of progenitor cells leading to neurogenesis and
Macrophage colony-stimulating factor is expressed in neuron and microglia after focal brain injury
✍ Scribed by Akihide Takeuchi; Osamu Miyaishi; Kazutoshi Kiuchi; Ken-ichi Isobe
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 525 KB
- Volume
- 65
- Category
- Article
- ISSN
- 0360-4012
- DOI
- 10.1002/jnr.1125
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✦ Synopsis
Abstract
In a previous study, we have demonstrated that damaged neurons within a boundary area around necrosis fall into delayed neuronal death owing to the cytotoxic effect of microglial nitric oxide (NO), and these neurons are finally eliminated by activated microglia. In this process, microglia are activated to release NO, increase in number, and accumulate toward the damaged area. In this study, we investigated the expression of macrophage colony‐stimulating factor (M‐CSF, also called colony stimulating factor‐1; CSF‐1) and other cytokines, which are reported to relate to activation, proliferation, or migration of microglia. The mRNA of M‐CSF arose biphasically from 30 min to 1 hr and from 6 to 72 hr after the injury, as demonstrated by semiquantitative RT‐PCR. However, another cytokine of granulocyte‐macrophage CSF (GM‐CSF) or interleukin‐3 (IL‐3), which causes proliferation of microglia in vitro, was not detected. From immunohistochemical studies, positive staining of M‐CSF was observed mainly in neuron‐specific enolase (NSE)‐positive cells from 1 to 12 hr after the injury, and after that M‐CSF became positive in Griffonia simplicifolia isolectin‐B4 (GSA‐I‐B4)‐positive cells from 24 to 72 hr in the boundary area around necrosis. These results suggest that neurons around the damaged area express M‐CSF in the early phase after injury, which may initially activate microglia, and these activated microglia also express M‐CSF later, causing further proliferation or migration of microglia themselves to eliminate damaged neurons or necrotic brain tissue. J. Neurosci. Res. 65:38–44, 2001. © 2001 Wiley‐Liss, Inc.
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