Excitotoxic injury induces production of monocyte chemoattractant protein-1 in rat cortico-striatal slice cultures
T Katayama, M Minami, M Nakamura, M Ito… - Neuroscience …, 2002 - Elsevier
Neuroscience letters, 2002•Elsevier
The effect of excitotoxic injury on the production of monocyte chemoattractant protein-1
(MCP-1) was examined in rat cortico-striatal slice cultures. Treatment with 50 μM N-methyl-d-
aspartate (NMDA) for 4 h, which caused severe damage in neurons, induced the production
of MCP-1 in astrocytes. Production levels were markedly elevated immediately after the
treatment, peaked at 4–8 h, and had decreased to nearly the basal level by 72 h. Since the
treatment promoted the release of MCP-1 in the slice cultures, but not in the enriched …
(MCP-1) was examined in rat cortico-striatal slice cultures. Treatment with 50 μM N-methyl-d-
aspartate (NMDA) for 4 h, which caused severe damage in neurons, induced the production
of MCP-1 in astrocytes. Production levels were markedly elevated immediately after the
treatment, peaked at 4–8 h, and had decreased to nearly the basal level by 72 h. Since the
treatment promoted the release of MCP-1 in the slice cultures, but not in the enriched …
The effect of excitotoxic injury on the production of monocyte chemoattractant protein-1 (MCP-1) was examined in rat cortico-striatal slice cultures. Treatment with 50 μM N-methyl-d-aspartate (NMDA) for 4 h, which caused severe damage in neurons, induced the production of MCP-1 in astrocytes. Production levels were markedly elevated immediately after the treatment, peaked at 4–8 h, and had decreased to nearly the basal level by 72 h. Since the treatment promoted the release of MCP-1 in the slice cultures, but not in the enriched astrocyte cultures, it is unlikely that NMDA directly acted on the astrocytes. These results suggest that information on neuronal injury induced by NMDA is transmitted to astrocytes to induce the production of MCP-1. Organotypic slice cultures are useful for investigating the inflammatory responses of astrocytes in the process of neuronal injury.
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