Nimodipine inhibits TMB-8 potentiation of AMPA-induced hippocampal neurodegeneration
Article first published online: 11 NOV 2008
Copyright © 2008 Wiley-Liss, Inc.
Journal of Neuroscience Research
Volume 87, Issue 5, pages 1240–1249, April 2009
How to Cite
Bernal, F., Petegnief, V., Rodríguez, M. J., Ursu, G., Pugliese, M. and Mahy, N. (2009), Nimodipine inhibits TMB-8 potentiation of AMPA-induced hippocampal neurodegeneration. J. Neurosci. Res., 87: 1240–1249. doi: 10.1002/jnr.21930
- Issue published online: 23 FEB 2009
- Article first published online: 11 NOV 2008
- Manuscript Revised: 3 SEP 2008
- Manuscript Accepted: 3 SEP 2008
- Manuscript Received: 13 FEB 2008
- Spanish Ministerio de Sanidad y Consumo (project CIBERNED)
- Spanish Ministerio de Educación y Ciencia. Grant Number: SAF2005-04314
- Generalitat de Catalunya. Grant Number: 2005SGR00609
Human cerebral calcification has been related to deregulation of intracellular calcium homeostasis. In rat basal ganglia, nimodipine and TMB-8, two commonly used calcium antagonists, worsen the chronic AMPA-induced lesion, whereas only nimodipine potentiates calcification. To investigate whether similar effects are present in the hippocampus, AMPA dose–response and calcium movement blockade were performed. A dose-related increase of both hippocampal lesion and calcification was evident in a saturable mode, mostly different from the continuous globus pallidus response previously observed. The value of 2.7 nmol AMPA, selected as yielding 60% of maximum calcification, was coinjected with nimodipine or/and TMB-8 to determine their influence on tissue damage. TMB-8 increased the AMPA lesion in terms of calcified area, and nimodipine reversed this increase, with no effect alone. These results, divergent from those for the globus pallidus, reveal differences in extra- and intracellular calcium movement between the two neurodegenerative processes. Future work focused on other brain areas is required to understand how control of calcium stores may influence neurodegenerative disease evolution. © 2008 Wiley-Liss, Inc.