Neuroprotection by estrogen via extracellular signal-regulated kinase against quinolinic acid-induced cell death in the rat hippocampus

Citation
Y. Kuroki et al., Neuroprotection by estrogen via extracellular signal-regulated kinase against quinolinic acid-induced cell death in the rat hippocampus, EUR J NEURO, 13(3), 2001, pp. 472-476
Citations number
26
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EUROPEAN JOURNAL OF NEUROSCIENCE
ISSN journal
0953-816X → ACNP
Volume
13
Issue
3
Year of publication
2001
Pages
472 - 476
Database
ISI
SICI code
0953-816X(200102)13:3<472:NBEVES>2.0.ZU;2-A
Abstract
Extracellular signal-regulated kinase (ERK) belongs to the family of mitoge n-activated protein kinases (MAPKs), which are serine-threonine kinases act ivated by phosphorylation in response to a variety of mitogenic signals. We previously reported that 17 beta -estradiol rapidly activates ERK in the r at hippocampus. However, the physiological role of this rapid activation of ERK by estrogen in vivo has not yet been elucidated. This study investigat ed whether ERK may participate in mediating the neuroprotective effects of estrogen against quinolinic acid (QA) toxicity in the rat hippocampus in vi vo. Injection of QA into the hippocampi of male rats produced a loss of Nis sl-stained neurons in the CA1 after 24 h. Prior administration of 17 beta - estradiol (50 pmol/animal) to the ventricles prevented the QA-induced decre ase in Nissl-stained neurons. Pretreatment with U0126, an inhibitor of MAPK /ERK kinase, inhibited the rapid activation of ERK by 17 beta -estradiol in the rat hippocampus. Moreover, the neuroprotective effects of 17 beta -est radiol against QA toxicity were blocked by the pretreatment with U0126. U01 26 alone did not produce a loss of neurons. These results indicate that ERK mediates estrogen neuroprotection after QA toxicity in the rat hippocampus .