Abstract
Kainic acid (KA) treatment induced neuronal death and apoptosis in murine cerebellar granule cells (CGNs) cultures from both wild-type and knockout p21(-/-) mice. There was not statistically significant difference in the percentage of neuronal apoptosis among strains. KA-induced neurotoxicity was prevented in the presence of NBQX (20 microM) and GYKI 52446 (20 microM), but not by z-VAD-fmk, suggesting that caspases are not involved in the apoptotic process. Data suggest that p21(WAF/Cip) was unable to modulate KA-induced apoptosis in murine CGNs.
Publication types
-
Comparative Study
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Apoptosis / drug effects
-
Apoptosis / physiology*
-
Benzodiazepines / pharmacology
-
Cell Cycle / drug effects
-
Cell Cycle / physiology*
-
Cell Cycle Proteins / genetics
-
Cell Cycle Proteins / physiology*
-
Cells, Cultured
-
Cerebellum / cytology
-
Cerebellum / drug effects
-
Cerebellum / metabolism*
-
Cyclin-Dependent Kinase Inhibitor p21
-
Excitatory Amino Acid Antagonists / pharmacology
-
Kainic Acid
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
-
Nerve Degeneration / chemically induced
-
Neurons / cytology
-
Neurons / drug effects
-
Neurons / metabolism*
-
Quinoxalines / pharmacology
-
Receptors, AMPA / antagonists & inhibitors
Substances
-
Cdkn1a protein, mouse
-
Cell Cycle Proteins
-
Cyclin-Dependent Kinase Inhibitor p21
-
Excitatory Amino Acid Antagonists
-
Quinoxalines
-
Receptors, AMPA
-
GYKI 52466
-
2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline
-
Benzodiazepines
-
Kainic Acid