 |
Previous Article | Next Article 
The Journal of Neuroscience, November 1, 1999, 19(21):9459-9468
Growth Factors and Taurine Protect against Excitotoxicity by
Stabilizing Calcium Homeostasis and Energy Metabolism
Abdeslem
El Idrissi and
Ekkhart
Trenkner
New York State Institute for Basic Research in Developmental
Disabilities, Center for Developmental Neuroscience, The Graduate
School and University Center of the City University of New York, Staten
Island, New York 10314
Taurine, brain derived neurotrophic factor (BDNF), and basic
fibroblast growth factor (bFGF) are known to control the development of
early postnatal cerebellar granule cells. This study attempted to
investigate possible mechanisms of this control by determining neuronal
survival, calcium homeostasis, and related calcium-mediated functions,
as well as the site of action during glutamate-induced excitotoxicity
in cultures of cerebellar granule cells. We report that stimulation of
glutamate receptors induced a rapid increase in intracellular calcium
concentrations ([Ca2+]i) and a
decrease in mitochondrial energy metabolism. These effects of glutamate
were time- and concentration-dependent and could be specifically
blocked by glutamate receptor antagonists. Taurine and bFGF but not
BDNF differently regulated
[Ca2+]i, and preserved the
mitochondrial energy metabolism in the presence of glutamate. The
regulation of [Ca2+]i by bFGF and
taurine required pretreatment of cells with these factors. Confocal
microscope analysis of [Ca2+]i and
45Ca2+ uptake studies showed that bFGF
reduced the magnitude of glutamate-induced calcium uptake with no
apparent regulation thereafter. Taurine, on the other hand, did not
affect the level of calcium uptake induced by glutamate but rather the
duration of the maximal response; this maximal response was transient
and returned to basal levels ~10 min after glutamate receptor
stimulation. We conclude from these data that bFGF and taurine prevent
glutamate excitotoxicity through regulation of
[Ca2+]i and mitochondrial energy
metabolism. Furthermore, the neuroprotective role of taurine and bFGF
was enhanced by their collaboration.
Key words:
cerebellar granule cells; excitotoxicity; growth factors; taurine; glutamate; calcium; energy metabolism; BDNF; bFGF
Copyright © 1999 Society for Neuroscience 0270-6474/99/19219459-10$05.00/0
This article has been cited by other articles:

|
 |

|
 |
 
Y. Zhu, J. M. Antony, J. A. Martinez, D. M. Glerum, V. Brussee, A. Hoke, D. Zochodne, and C. Power
Didanosine causes sensory neuropathy in an HIV/AIDS animal model: impaired mitochondrial and neurotrophic factor gene expression
Brain,
August 1, 2007;
130(8):
2011 - 2023.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
I. Morales, J. G. Dopico, M. Sabate, T. Gonzalez-Hernandez, and M. Rodriguez
Substantia nigra osmoregulation: taurine and ATP involvement
Am J Physiol Cell Physiol,
May 1, 2007;
292(5):
C1934 - C1941.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. Studenski, M. C. Carlson, H. Fillit, W. T. Greenough, A. Kramer, and G. W. Rebok
From Bedside to Bench: Does Mental and Physical Activity Promote Cognitive Vitality in Late Life?
Sci. Aging Knowl. Environ.,
June 28, 2006;
2006(10):
pe21 - pe21.
[Abstract]
[Full Text]
|
 |
|

|
 |

|
 |
 
S. Vaynman and F. Gomez-Pinilla
License to Run: Exercise Impacts Functional Plasticity in the Intact and Injured Central Nervous System by Using Neurotrophins
Neurorehabil Neural Repair,
December 1, 2005;
19(4):
283 - 295.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
F. Li, I. G. Obrosova, O. Abatan, D. Tian, D. Larkin, E. L. Stuenkel, and M. J. Stevens
Taurine replacement attenuates hyperalgesia and abnormal calcium signaling in sensory neurons of STZ-D rats
Am J Physiol Endocrinol Metab,
January 1, 2005;
288(1):
E29 - E36.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
P. R. LOUZADA, A. C. P. LIMA, D. L. MENDONCA-SILVA, F. NOEL, F. G. DE MELLO, and S. T. FERREIRA
Taurine prevents the neurotoxicity of {beta}-amyloid and glutamate receptor agonists: activation of GABA receptors and possible implications for Alzheimer's disease and other neurological disorders
FASEB J,
March 1, 2004;
18(3):
511 - 518.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|