Alterations in metabolism and gap junction expression may determine the role of astrocytes as "Good samaritans" or executioners

被引:81
作者
Farahani, R
Pina-Benabou, MH
Kyrozis, A
Siddiq, A
Barradas, PC
Chiu, FC
Cavalcante, LA
Lai, JCK
Stanton, PK
Rozental, R
机构
[1] New York Med Coll, Dept Cell Biol & Anat, Valhalla, NY 10595 USA
[2] Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10467 USA
[3] Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10467 USA
[4] Univ Estado Rio de Janeiro, Inst Biol Roberto Alcantara Gomes, Rio De Janeiro, Brazil
[5] Med Coll Georgia, Inst Mol Med & Genet, Augusta, GA 30912 USA
[6] Univ Fed Rio de Janeiro, Inst Biofis Carlos Chagas Filho, BR-21941 Rio De Janeiro, Brazil
[7] Idaho State Univ, Coll Pharm, Dept Pharmaceut Sci, Pocatello, ID 83209 USA
[8] New York Med Coll, Dept Neurol, Valhalla, NY 10595 USA
[9] New York Med Coll, Dept Obstet & Anesthesiol, Valhalla, NY 10595 USA
关键词
astrocyte; gap junctions; metabolism; connexin43; bystander effect; hypoxia-ischemia;
D O I
10.1002/glia.20213
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Our knowledge of astroglia and their physiological and pathophysiological role(s) in the central nervous system (CNS) has grown during the past decade, revealing a complex picture. It is becoming increasingly clear that glia play a significant role in the homeostasis and function of the CNS and that neurons should no longer be considered the only cell type that responds, both rapidly and slowly, to electrochemical activity. We discuss recent advances in the field with an emphasis on the impact of hypoxia and ischemia on astrocytic metabolism and the functional relationship between glucose metabolism and gap junctions in astrocytes. We also address the controversy over whether astrocytic gap junctions mediate protection or killing of neurons during or after hypoxic or ischemic insults. (c) 2005 Wiley-Liss, Inc.
引用
收藏
页码:351 / 361
页数:11
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