Estrogens: Trophic and protective factors in the adult brain

被引:191
作者
Wise, PM [1 ]
Dubal, DB [1 ]
Wilson, ME [1 ]
Rau, SW [1 ]
Liu, Y [1 ]
机构
[1] Univ Kentucky, Coll Med, Dept Physiol, Lexington, KY 40536 USA
关键词
estrogen; estradiol; neuroprotection; injury; cell death; brain; cerebral cortex; hippocampus;
D O I
10.1006/frne.2000.0207
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Our appreciation that estrogens are important neurotrophic and neuroprotective factors has grown rapidly. Although a thorough understanding of the molecular and cellular mechanisms that underlie this effect requires further investigation, significant progress has been made due to the availability of animal models in which we can test potential candidates. It appears that estradiol can act via mechanisms that require classical intracellular receptors (estrogen receptor alpha or beta) that affect transcription, via mechanisms that include cross-talk between estrogen receptors and second messenger pathways, and/or via mechanisms that may involve membrane receptors or channels. This area of research demands attention since estradiol may be an important therapeutic agent in the maintenance of normal neural function during aging and after injury. (C) 2001 Academic Press.
引用
收藏
页码:33 / 66
页数:34
相关论文
共 251 条
[1]   Gender-linked brain injury in experimental stroke [J].
Alkayed, NJ ;
Harukuni, I ;
Kimes, AS ;
London, ED ;
Traystman, RJ ;
Hurn, PD .
STROKE, 1998, 29 (01) :159-165
[2]   ANDROGEN ENHANCES NEURONAL DEGENERATION IN THE DEVELOPING PREOPTIC AREA - APOPTOSIS IN THE ANTEROVENTRAL PERIVENTRICULAR NUCLEUS (AVPVN-POA) [J].
ARAI, Y ;
MURAKAMI, S ;
NISHIZUKA, M .
HORMONES AND BEHAVIOR, 1994, 28 (04) :313-319
[3]   ESTROGEN-TREATMENT ENHANCES SURVIVAL OF CULTURED FETAL-RAT AMYGDALA NEURONS IN A DEFINED MEDIUM [J].
ARIMATSU, Y ;
HATANAKA, H .
DEVELOPMENTAL BRAIN RESEARCH, 1986, 26 (01) :151-159
[4]   Ethinylestradiol does not enhance the expression of nitric oxide synthase in bovine endothelial cells but increases the release of bioactive nitric oxide by inhibiting superoxide anion production [J].
Arnal, JF ;
Clamens, S ;
Pechet, C ;
NegreSalvayre, A ;
Allera, C ;
Girolami, JP ;
Salvayre, R ;
Bayard, F .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (09) :4108-4113
[5]   Cognitive and neuroendocrine response to transdermal estrogen in postmenopausal women with Alzheimer's disease: results of a placebo-controlled, double-blind, pilot study [J].
Asthana, S ;
Craft, S ;
Baker, LD ;
Raskind, MA ;
Birnbaum, RS ;
Lofgreen, CP ;
Veith, RC ;
Plymate, SR .
PSYCHONEUROENDOCRINOLOGY, 1999, 24 (06) :657-677
[6]  
Azcoitia I, 1999, J NEUROSCI RES, V58, P815, DOI 10.1002/(SICI)1097-4547(19991215)58:6<815::AID-JNR8>3.0.CO
[7]  
2-R
[8]   ESTROGEN AND CORONARY HEART-DISEASE IN WOMEN [J].
BARRETTCONNOR, E ;
BUSH, TL .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1991, 265 (14) :1861-1867
[9]   ESTROGEN REPLACEMENT THERAPY AND COGNITIVE FUNCTION IN OLDER WOMEN [J].
BARRETTCONNOR, E ;
KRITZSILVERSTEIN, D .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1993, 269 (20) :2637-2641
[10]  
BARRETTCONNOR E, 2000, BRIT MED J, V317, P457