Abstract
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.
Original language | English (US) |
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Pages (from-to) | 63-68 |
Number of pages | 6 |
Journal | Neurobiology of Disease |
Volume | 59 |
DOIs | |
State | Published - Nov 2013 |
Keywords
- Astrocyte
- Cytokine
- Inflammation
- Interleukin-6
- Schizophrenia
ASJC Scopus subject areas
- Neurology