Protective effect of parvalbumin on excitotoxic motor neuron death

Experimental Neurology
Ludo Van Den BoschM W Berchtold

Abstract

The mechanism responsible for the selective vulnerability of motor neurons in amyotrophic lateral sclerosis (ALS) is poorly understood. Several lines of evidence indicate that susceptibility of motor neurons to Ca(2+) overload induced by excitotoxic stimuli is involved. In this study, we investigated whether the high density of Ca(2+)-permeable AMPA receptors on motor neurons gives rise to higher Ca(2+) transients in motor neurons compared to dorsal horn neurons. Dorsal horn neurons were chosen as controls as these cells do not degenerate in ALS. In cultured spinal motor neurons, the rise of the cytosolic Ca(2+) concentration induced by kainic acid (KA) and mediated by the AMPA receptor was almost twice as high as in spinal neurons from the dorsal horn. Furthermore, we investigated whether increasing the motor neuron's cytosolic Ca(2+)-buffering capacity protects them from excitotoxic death. To obtain motor neurons with increased Ca(2+) buffering capacity, we generated transgenic mice overexpressing parvalbumin (PV). These mice have no apparent phenotype. PV overexpression was present in the central nervous system, kidney, thymus, and spleen. Motor neurons from these transgenic mice expressed PV in culture and were partially pr...Continue Reading

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Citations

May 23, 2012·Pflügers Archiv : European journal of physiology·Michael R Duchen
Oct 15, 2010·Cold Spring Harbor Perspectives in Biology·Beat Schwaller
Aug 16, 2006·Neuro-degenerative Diseases·P Van DammeL Van Den Bosch
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Sep 7, 2007·Proceedings of the National Academy of Sciences of the United States of America·Philip Van DammeWim Robberecht
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Jan 24, 2007·Cell Calcium·Julian GrosskreutzLudo Van Den Bosch
Jun 10, 2010·The European Journal of Neuroscience·André Bento-AbreuWim Robberecht
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Jun 23, 2005·Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology·Toshiki HimedaTsutomu Araki

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