PMID- 10531449
OWN - NLM
STAT- MEDLINE
DCOM- 19991119
LR  - 20220317
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 19
IP  - 21
DP  - 1999 Nov 1
TI  - Growth factors and taurine protect against excitotoxicity by stabilizing calcium 
      homeostasis and energy metabolism.
PG  - 9459-68
AB  - 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 ([Ca(2+)](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 [Ca(2+)](i), and 
      preserved the mitochondrial energy metabolism in the presence of glutamate. The 
      regulation of [Ca(2+)](i) by bFGF and taurine required pretreatment of cells with 
      these factors. Confocal microscope analysis of [Ca(2+)](i) and (45)Ca(2+) 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 approximately 10 min after glutamate receptor 
      stimulation. We conclude from these data that bFGF and taurine prevent glutamate 
      excitotoxicity through regulation of [Ca(2+)](i) and mitochondrial energy 
      metabolism. Furthermore, the neuroprotective role of taurine and bFGF was 
      enhanced by their collaboration.
FAU - El Idrissi, A
AU  - El Idrissi A
AD  - New York State Institute for Basic Research, Center for Developmental Mei of the 
      City University of New York, Staten Island, New York 10314, USA.
FAU - Trenkner, E
AU  - Trenkner E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Culture Media)
RN  - 0 (Neurotoxins)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - 11P2JDE17B (beta-Alanine)
RN  - 1EQV5MLY3D (Taurine)
RN  - 3KX376GY7L (Glutamic Acid)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Biological Transport
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Calcium/*metabolism
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Cerebellum/cytology/*physiology
MH  - Coculture Techniques
MH  - Culture Media
MH  - Energy Metabolism/drug effects/*physiology
MH  - Fibroblast Growth Factor 2/*pharmacology
MH  - Glutamic Acid/*toxicity
MH  - Homeostasis/drug effects
MH  - Kinetics
MH  - Mice
MH  - Mitochondria/drug effects/*metabolism
MH  - Neurons/classification/cytology/*physiology
MH  - Neurotoxins/*toxicity
MH  - Taurine/*pharmacology
MH  - beta-Alanine/pharmacology
PMC - PMC6782936
EDAT- 1999/10/26 00:00
MHDA- 1999/10/26 00:01
PMCR- 2000/05/01
CRDT- 1999/10/26 00:00
PHST- 1999/10/26 00:00 [pubmed]
PHST- 1999/10/26 00:01 [medline]
PHST- 1999/10/26 00:00 [entrez]
PHST- 2000/05/01 00:00 [pmc-release]
AID - 3584 [pii]
AID - 10.1523/JNEUROSCI.19-21-09459.1999 [doi]
PST - ppublish
SO  - J Neurosci. 1999 Nov 1;19(21):9459-68. doi: 10.1523/JNEUROSCI.19-21-09459.1999.