Intracerebral trafficking of lactate in vivo during stress, exercise, electroconvulsive shock and ischemia as studied with microdialysis.
We developed techniques to continuously monitor lactate in the living rat ('lactography') based on microdialysis and on-line enzymatic conversion of lactate in the dialysate using either continuous flow technologies or enzyme reactors. In vivo lactate was monitored during a single electroconvulsive shock, stress, swimming, repetitive hypoxia and after local infusion of probenecid (a blocker of carrier-mediated lactate transport) 1 or 2 days after implantation of the microdialysis probe. In a few experiments the rats were also perfused 1-2 weeks after surgery, so glial function predominates, because of gliosis around the probe. Our experiments indicate that extracellular lactate increases during stress, convulsion or exercise (particularly in the rat hippocampus), it is cleared from the extracellular space by a carrier-mediated mechanism and originates in glial cells at least in part. These in vivo studies support the concept of metabolic trafficking of lactate between glia cells and neurons.
Korf
J
J
Department of Biological Psychiatry, Groningen University, The Netherlands.
D000818:Animals; D001522:Behavior, Animal; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D004563:Electrochemistry / Q000379:methods; D004597:Electroshock; D019344:Lactic Acid / Q000378:metabolism*; D008297:Male; D017551:Microdialysis; D009457:Neuroglia / Q000378:metabolism; D005082:Physical Exertion; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000378:metabolism*
D019344:Lactic Acid