Hypoglycemia, brain energetics, and hypoglycemic neuronal death

被引:146
作者
Suh, Sang Won
Hamby, Aaron M.
Swanson, Raymond A.
机构
[1] Vet Affairs Med Ctr, San Francisco, CA 94121 USA
[2] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA
关键词
glucose; zinc; astrocyte; PARP-1; glycogen; energy; EEG;
D O I
10.1002/glia.20440
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Hypoglycemia is a common and serious problem among diabetic patients receiving treatment with insulin or other glucose-lowering drugs. Moderate hypoglycemia impairs neurological function, and severe hypoglycemia leads to death of selectively vulnerable neurons. Recent advances have shed new light on the underlying processes that cause neuronal death in hypoglycemia and the factors that may render specific neuronal populations especially vulnerable to hypoglycemia. In addition to its clinical importance, the pathophysiology of hypoglycemia is an indicator of the unique bioenergetic properties of the central nervous system, in particular the metabolic coupling of neuronal and astrocyte metabolism. This review will focus on relationships between bioenergetics and brain dysfunction in hypoglycemia, the neuronal cell death program triggered by hypoglycemia, and the role of astrocytes in these processes. (C) 2007 Wiley-Liss, Inc.
引用
收藏
页码:1280 / 1286
页数:7
相关论文
共 101 条
[91]   POSSIBLE ROLE OF ZINC IN THE SELECTIVE DEGENERATION OF DENTATE HILAR NEURONS AFTER CEREBRAL-ISCHEMIA IN THE ADULT-RAT [J].
TONDER, N ;
JOHANSEN, FF ;
FREDERICKSON, CJ ;
ZIMMER, J ;
DIEMER, NH .
NEUROSCIENCE LETTERS, 1990, 109 (03) :247-252
[92]   A1 adenosine receptors mediate hypoglycemia-induced neuronal injury [J].
Turner, CP ;
Blackburn, MR ;
Rivkees, SA .
JOURNAL OF MOLECULAR ENDOCRINOLOGY, 2004, 32 (01) :129-144
[93]   Glucose deprivation produces a prolonged increase in sensitivity to glutamate in cultured rat cortical neurons [J].
Vergun, O ;
Han, YY ;
Reynolds, IJ .
EXPERIMENTAL NEUROLOGY, 2003, 183 (02) :682-694
[94]   Astrocytic glycogen influences axon function and survival during glucose deprivation in central white matter [J].
Wender, R ;
Brown, AM ;
Fern, R ;
Swanson, RA ;
Farrell, K ;
Ransom, BR .
JOURNAL OF NEUROSCIENCE, 2000, 20 (18) :6804-6810
[95]   HYPOGLYCEMIA-INDUCED NEURONAL DAMAGE PREVENTED BY AN N-METHYL-D-ASPARTATE ANTAGONIST [J].
WIELOCH, T .
SCIENCE, 1985, 230 (4726) :681-683
[96]   LESIONS OF THE GLUTAMATERGIC CORTICO-STRIATAL PROJECTIONS IN THE RAT AMELIORATE HYPOGLYCEMIC BRAIN-DAMAGE IN THE STRIATUM [J].
WIELOCH, T ;
ENGELSEN, B ;
WESTERBERG, E ;
AUER, R .
NEUROSCIENCE LETTERS, 1985, 58 (01) :25-30
[97]   Repetitive hypoglycemia in young rats impairs hippocampal long-term potentiation [J].
Yamada, KA ;
Rensing, N ;
Izumi, Y ;
De Erausquin, GA ;
Gazit, V ;
Dorsey, DA ;
Herrera, DG .
PEDIATRIC RESEARCH, 2004, 55 (03) :372-379
[98]   NAD+ repletion prevents PARP-1-induced glycolytic blockade and cell death in cultured mouse astrocytes [J].
Ying, WH ;
Garnier, P ;
Swanson, RA .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2003, 308 (04) :809-813
[99]   Mediation of poly(ADP-ribose) polymerase-1-dependent cell death by apoptosis-inducing factor [J].
Yu, SW ;
Wang, HM ;
Poitras, MF ;
Coombs, C ;
Bowers, WJ ;
Federoff, HJ ;
Poirier, GG ;
Dawson, TM ;
Dawson, VL .
SCIENCE, 2002, 297 (5579) :259-263
[100]   ADENOSINE RELEASE IS A MAJOR CAUSE OF FAILURE OF SYNAPTIC TRANSMISSION DURING HYPOGLYCEMIA IN RAT HIPPOCAMPAL SLICES [J].
ZHU, PJ ;
KRNJEVIC, K .
NEUROSCIENCE LETTERS, 1993, 155 (02) :128-131