Journal
JOURNAL OF MOLECULAR NEUROSCIENCE
Volume 55, Issue 3, Pages 596-608Publisher
HUMANA PRESS INC
DOI: 10.1007/s12031-014-0398-0
Keywords
P38 MAPK; Glutamate; Excitotoxicity; Glu-R expression; Cell signaling
Categories
Funding
- CONACYT [177594]
Ask authors/readers for more resources
NMDA and AMPA receptors are thought to be responsible for Ca++ influx during glutamate-induced excitotoxicity and, therefore, hippocampal neuronal death. We assessed whether excitotoxicity induced by neonatal treatment with monosodium glutamate in rats at postnatal age of 1, 3, 5, and 7 modifies the hippocampal expression of the NMDAR subunit NR1 and the AMPAR subunits GluR1/GluR2 at postnatal days 8, 10, 12, and 14. We also assessed the involvement of MAPK signaling by using the p38 inhibitor SB203580. Our results showed that monosodium glutamate induces neuronal death and alters the expression of the subunits evaluated in the hippocampus at all ages studied, which could be prevented by SB203580 treatment. Furthermore, expression of the NRSF gene silencing factor also increased in response to excitotoxicity, suggesting a relationship in suppressing GluR2-expression, which was regulated by the p38-MAPK pathway inhibitor SB203580. This result suggests that selectively blocking the pro-death signaling pathway may reduce neuronal death in some neuro-degenerative diseases in which these neurotoxic processes are present and produce major clinical benefits in the treatment of these pathologies.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available