Survival of energy failure in the anoxic frog brain: delayed release of glutamate.
This study investigated the relationship between energy failure and neurotransmitter release in the frog (Rana pipiens) brain during 1-3 h of anoxia. Unlike truly anoxia-tolerant species, the frog does not defend its brain energy charge. When exposed to anoxia at 25 degrees C, there is an immediate fall in brain ATP levels, which reach approximately 20% of normoxic levels in approximately 60 min. The frog, nevertheless, survives another 1-2 h of anoxia. At 100 min of anoxia, there is an increase in extracellular adenosine concentration, probably originating from the increased intracellular adenosine concentration caused by the breakdown of intracellular ATP. Increases in the levels of extracellular glutamate and GABA do not occur until 1-2 h after ATP depletion. This response is quite unlike that recorded for other vertebrates, anoxia-tolerant or anoxia-intolerant, where energy failure quickly results in an uncontrolled and neurotoxic release of excitatory neurotransmitters. In the frog, the delay in excitotoxic neurotransmitter release may be one of the factors that allow a period of survival after energy failure. Clearly, energy failure by itself is not a fatal event in the frog brain.
Lutz
P L
PL
Department of Biological Sciences, Florida Atlantic University, Boca Raton 33149, USA. lutz@acc.fau.edu
Reiners
R
R
D000222:Adaptation, Physiological; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D004734:Energy Metabolism; D018698:Glutamic Acid / Q000378:metabolism*; D002534:Hypoxia, Brain / Q000378:metabolism / Q000503:physiopathology*; D017136:Ion Transport; D011894:Rana pipiens / Q000502:physiology*; D013045:Species Specificity; D013997:Time Factors
D018698:Glutamic Acid; D000255:Adenosine Triphosphate; D002118:Calcium