Vertebrate brains at the pilot light

被引:68
作者
Lutz, PL [1 ]
Nilsson, GE
机构
[1] Florida Atlantic Univ, Dept Sci Biol, Boca Raton, FL 33431 USA
[2] Dept Biol, Div Gen Physiol, N-0316 Oslo, Norway
关键词
anoxia; tolerance; hypoxia; brain; metabolism;
D O I
10.1016/j.resp.2004.03.013
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
While the brains of most vertebrates are unable to tolerate more than a few minutes of anoxia, some freshwater turtles (Trachemys and Chrysemys), crucian carp (Carassius carassius) and frogs (Rana pipens and Rana temporaria) can survive anoxia for hours to months. Obviously, anoxia tolerance has evolved separately several times and this is also reflected in the divergent strategies these animals utilize to survive without oxygen. The turtles and crucian carp defend their brain ATP levels and avoid a loss of ion homeostasis by reducing ATP use. In the turtles, the early release of adenosine and the activation of K-ATP channels, a progressive release of GABA and a drastic reduction in electric activity and ion fluxes send the brain into a comatose like state. The crucian carp displays a more modest depression of ATP use, probably achieved through a moderated release of GABA and adenosine, allowing the animal to maintain physical activity in anoxia. The anoxic frog, on the other hand, seems to rely on mechanisms that greatly retard the anoxia induced fall in ATP levels and loss of ion homeostasis, so that the brain can be saved as long as the anoxia is limited to a few hours. The sequence of events characterizing the anoxic frog brain is similar to that of failing anoxic mammalian brain, although over a greatly extended time frame, allowing the frog to die slowly in anoxia, rather than survive. By contrast the only factor that limits anoxic survival in turtles and crucian carp may be the final depletion of their glycogen reserves. (C) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:285 / 296
页数:12
相关论文
共 70 条
[1]   Hypoxia-induced silencing of NMDA receptors in turtle neurons [J].
Bickler, PE ;
Donohoe, PH ;
Buck, LT .
JOURNAL OF NEUROSCIENCE, 2000, 20 (10) :3522-3528
[2]   Mechanisms of metabolic defense against hypoxia in hibernating frogs [J].
Boutilier, RG .
RESPIRATION PHYSIOLOGY, 2001, 128 (03) :365-377
[3]  
Buck LT, 1998, J EXP BIOL, V201, P289
[4]   AIR GULPING IMPROVES BLOOD-OXYGEN TRANSPORT DURING AQUATIC-HYPOXIA IN THE GOLDFISH CARASSIUS AURATUS [J].
BURGGREN, WW .
PHYSIOLOGICAL ZOOLOGY, 1982, 55 (04) :327-334
[5]   ION LEAKAGE IS REDUCED DURING ANOXIA IN TURTLE BRAIN - A POTENTIAL SURVIVAL STRATEGY [J].
CHIH, CP ;
ROSENTHAL, M ;
SICK, TJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (06) :R1562-R1564
[6]   Characterization of transient focal ischemia-induced increases in extracellular glutamate and aspartate in spontaneously hypertensive rats [J].
Dawson, LA ;
Djali, S ;
Gonzales, C ;
Vinegra, MA ;
Zaleska, MM .
BRAIN RESEARCH BULLETIN, 2000, 53 (06) :767-776
[7]   SUBCELLULAR ENZYME BINDING AND THE REGULATION OF GLYCOLYSIS IN ANOXIC TURTLE BRAIN [J].
DUNCAN, JA ;
STOREY, KB .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 262 (03) :R517-R523
[8]   RELATIONSHIP BETWEEN ENERGY-EXPENDITURE AND ION CHANNEL DENSITY IN THE TURTLE AND RAT-BRAIN [J].
EDWARDS, RA ;
LUTZ, PL ;
BADEN, DG .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (06) :R1354-R1358
[9]  
Fraser KPP, 2001, J EXP BIOL, V204, P4353
[10]   ROLE OF DOPAMINE IN ISCHEMIC NEURONAL DAMAGE [J].
GLOBUS, MY .
STROKE, 1989, 20 (06) :827-828