The effects of glutamate can be attenuated by estradiol via estrogen receptor dependent pathway in rat adrenal pheochromocytoma cells.
Estrogens have been suggested to exhibit neuroprotective activities against several insults including beta-amyloid and glutamate, one of the excitatory neurotransmitters in the central nervous system. In the present study, we showed that exposure to glutamate not only inhibited the cell growth of exponentially growing rat pheochromocytoma PC12 cells in a time- and dose-dependent manner, but also influenced cell adherence capacity. Glutamate-induced growth inhibition was significantly attenuated by the co-administration of estradiol in PC12 cells. Pre-exposure of the PC12 cells to the estradiol was not required for protection against glutamate-induced growth inhibition. Administration of anti-estrogen ICI182,780 efficiently blocked the neuroprotective effects of estradiol. Glutamate-induced changes in cell adherence, on the other hand, were not significantly affected by estradiol. These data indicate that the neuroprotective effects of estradiol against glutamate-induced insults in PC12 cells, at least in part, involve estrogen receptor-dependent pathways.
Chan
Ching-Rong
CR
Department of Microbiology, Soochow University, Taipei, Taiwan, ROC.
Hsu
Jih-Tay
JT
Chang
I-tea
IT
Young
Y-C
YC
Lin
Chun-Ming
CM
Ying
Chingwen
C
D000818:Animals; D004958:Estradiol / Q000502:physiology*; D018698:Glutamic Acid / Q000502:physiology*; D009420:Nervous System / Q000254:growth & development*; D016716:PC12 Cells; D051381:Rats; D011960:Receptors, Estrogen / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology
D011960:Receptors, Estrogen; D018698:Glutamic Acid; D004958:Estradiol
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