Journal
NEUROBIOLOGY OF DISEASE
Volume 59, Issue -, Pages 63-68Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2013.07.003
Keywords
Inflammation; Astrocyte; Cytokine; Interleukin-6; Schizophrenia
Categories
Funding
- Mitsubishi Tanabe Parma Corporation, U.S. Public Health Service [MH-069853]
- Silvio O. Conte Center grant [MH-094268, MH-084018, MH-088753, MH-085226, MH-092443]
- SMRI
- RUSK
- MSCRF
- NARSAD
- Uehara Memorial Foundation
- Kanae Foundation
- JSPS
- NIMH [MH-093458]
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A growing body of evidence suggests the involvement of inflammatory processes in the pathophysiology of schizophrenia. Four- to 8-week exposure-to cuprizone, a copper chelator, causes robust demyelination and has been used to build a model for multiple sclerosis. In contrast, we report here the effects of 1-week cuprizone exposure in mice. This short-term cuprizone exposure elicits behavioral changes that include augmented responsiveness to methamphetamine and phencyclidine, as well as impaired working memory. The cellular effects of 1-week cuprizone exposure differ substantially from the longer-term exposure; perturbation of astrocytes and microglia is induced without any sign of demyelination. Furthermore, the proinflammatory cytokine interleukin-6 was significantly up-regulated in glial fibrillary acidic protein (GFAP)-positive cells. We propose that this cuprizone short-term exposure may offer a model to study some aspects of biology relevant to schizophrenia and related conditions. (C) 2013 Published by Elsevier Inc.
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