Estrogen protects primary cortical neurons from glutamate toxicity

Cherie A. Singer, Keith L. Rogers, Tamara M. Strickland, Daniel Dorsa

Research output: Contribution to journalArticle

282 Citations (Scopus)

Abstract

The gonadal steroid estrogen has been shown to affect neuronal growth, differentiation and survival. We examined the ability of estrogen to protect primary cortical neurons from toxicity induced by the excitatory neurotransmitter glutamate. In these experiments, a 24-h pretreatment with 15 and 50 nM 17β-estradiol significantly reduced cellular lactate dehydrogenase (LDH) release from primary cortical neurons, indicating that neurons treated with 17β-estradiol were protected from a toxic glutamate exposure. Pretreatment with related steroids such as progesterone, dihydrotestosterone, dexamethasone or cholesterol did not significantly decrease LDH release. The anti-estrogen tamoxifen blocked the protective effects of 17β-estradiol suggesting that a classical steroid hormone receptor may be involved in the mechanism subserving estrogen neuroprotection during glutamate toxicity.

Original languageEnglish (US)
Pages (from-to)13-16
Number of pages4
JournalNeuroscience Letters
Volume212
Issue number1
DOIs
StatePublished - Jul 5 1996
Externally publishedYes

Fingerprint

Glutamic Acid
Estrogens
Neurons
Estradiol
L-Lactate Dehydrogenase
Steroids
Dihydrotestosterone
Steroid Receptors
Poisons
Tamoxifen
Dexamethasone
Progesterone
Neurotransmitter Agents
Cholesterol
Hormones
Growth

Keywords

  • Cortex
  • Estrogen
  • Excitotoxicity
  • Neuroprotection

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Estrogen protects primary cortical neurons from glutamate toxicity. / Singer, Cherie A.; Rogers, Keith L.; Strickland, Tamara M.; Dorsa, Daniel.

In: Neuroscience Letters, Vol. 212, No. 1, 05.07.1996, p. 13-16.

Research output: Contribution to journalArticle

Singer, Cherie A. ; Rogers, Keith L. ; Strickland, Tamara M. ; Dorsa, Daniel. / Estrogen protects primary cortical neurons from glutamate toxicity. In: Neuroscience Letters. 1996 ; Vol. 212, No. 1. pp. 13-16.
@article{7d637dbb8bda475288af027286280c1b,
title = "Estrogen protects primary cortical neurons from glutamate toxicity",
abstract = "The gonadal steroid estrogen has been shown to affect neuronal growth, differentiation and survival. We examined the ability of estrogen to protect primary cortical neurons from toxicity induced by the excitatory neurotransmitter glutamate. In these experiments, a 24-h pretreatment with 15 and 50 nM 17β-estradiol significantly reduced cellular lactate dehydrogenase (LDH) release from primary cortical neurons, indicating that neurons treated with 17β-estradiol were protected from a toxic glutamate exposure. Pretreatment with related steroids such as progesterone, dihydrotestosterone, dexamethasone or cholesterol did not significantly decrease LDH release. The anti-estrogen tamoxifen blocked the protective effects of 17β-estradiol suggesting that a classical steroid hormone receptor may be involved in the mechanism subserving estrogen neuroprotection during glutamate toxicity.",
keywords = "Cortex, Estrogen, Excitotoxicity, Neuroprotection",
author = "Singer, {Cherie A.} and Rogers, {Keith L.} and Strickland, {Tamara M.} and Daniel Dorsa",
year = "1996",
month = "7",
day = "5",
doi = "10.1016/0304-3940(96)12760-9",
language = "English (US)",
volume = "212",
pages = "13--16",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

TY - JOUR

T1 - Estrogen protects primary cortical neurons from glutamate toxicity

AU - Singer, Cherie A.

AU - Rogers, Keith L.

AU - Strickland, Tamara M.

AU - Dorsa, Daniel

PY - 1996/7/5

Y1 - 1996/7/5

N2 - The gonadal steroid estrogen has been shown to affect neuronal growth, differentiation and survival. We examined the ability of estrogen to protect primary cortical neurons from toxicity induced by the excitatory neurotransmitter glutamate. In these experiments, a 24-h pretreatment with 15 and 50 nM 17β-estradiol significantly reduced cellular lactate dehydrogenase (LDH) release from primary cortical neurons, indicating that neurons treated with 17β-estradiol were protected from a toxic glutamate exposure. Pretreatment with related steroids such as progesterone, dihydrotestosterone, dexamethasone or cholesterol did not significantly decrease LDH release. The anti-estrogen tamoxifen blocked the protective effects of 17β-estradiol suggesting that a classical steroid hormone receptor may be involved in the mechanism subserving estrogen neuroprotection during glutamate toxicity.

AB - The gonadal steroid estrogen has been shown to affect neuronal growth, differentiation and survival. We examined the ability of estrogen to protect primary cortical neurons from toxicity induced by the excitatory neurotransmitter glutamate. In these experiments, a 24-h pretreatment with 15 and 50 nM 17β-estradiol significantly reduced cellular lactate dehydrogenase (LDH) release from primary cortical neurons, indicating that neurons treated with 17β-estradiol were protected from a toxic glutamate exposure. Pretreatment with related steroids such as progesterone, dihydrotestosterone, dexamethasone or cholesterol did not significantly decrease LDH release. The anti-estrogen tamoxifen blocked the protective effects of 17β-estradiol suggesting that a classical steroid hormone receptor may be involved in the mechanism subserving estrogen neuroprotection during glutamate toxicity.

KW - Cortex

KW - Estrogen

KW - Excitotoxicity

KW - Neuroprotection

UR - http://www.scopus.com/inward/record.url?scp=0030570392&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030570392&partnerID=8YFLogxK

U2 - 10.1016/0304-3940(96)12760-9

DO - 10.1016/0304-3940(96)12760-9

M3 - Article

VL - 212

SP - 13

EP - 16

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 1

ER -