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The Journal of Neuroscience, April 1, 1999, 19(7):2455-2463
The Mitogen-Activated Protein Kinase Pathway Mediates
Estrogen Neuroprotection after Glutamate Toxicity in Primary
Cortical Neurons
Cherie A.
Singer1,
Xavier A.
Figueroa-Masot3,
Robert H.
Batchelor1, and
Daniel M.
Dorsa1, 2
Departments of 1 Pharmacology and
2 Psychiatry and Behavioral Sciences and
3 Graduate Program in Neurobiology and Behavior, University
of Washington, Seattle, Washington 98195
Pharmacological and biochemical approaches were used to elucidate
the involvement of growth factor signaling pathways mediating estrogen
neuroprotection in primary cortical neurons after glutamate excitotoxicity. We addressed the activation of mitogen-activated protein kinase (MAPK) signaling pathways, which are activated by growth
factors such as nerve growth factor (NGF). Inhibition of MAPK signaling
with the MAPK kinase inhibitor PD98059 blocks both NGF and estrogen
neuroprotection in these neurons. These results correlate with a rapid
and sustained increase in MAPK activity within 30 min of estrogen
exposure. The involvement of signaling molecules upstream from MAPK was
also examined to determine whether activation of MAPK by estrogen is
mediated by tyrosine kinase activity. Estrogen produces a rapid,
transient activation of src-family tyrosine kinases and tyrosine
phosphorylation of p21ras-guanine nucleotide
activating protein. Effects of estrogen on neuroprotection, as well as
rapid activation of tyrosine kinase and MAPK activity, are blocked by
the anti-estrogen ICI 182,780. This provides evidence that activation
of the MAPK pathway by estrogen participates in mediating
neuroprotection via an estrogen receptor. These results describe a
novel mechanism by which cytoplasmic actions of the estrogen receptor
may activate the MAPK pathway, thus broadening the understanding of
effects of estrogen in neurons.
Key words:
estrogen; MAPK; neuroprotection; growth factors; excitotoxicity; src; GAP
Copyright © 1999 Society for Neuroscience 0270-6474/99/1972455-09$05.00/0
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