Regional distribution and extracellular levels of amino acids in rat central nervous system

Abstract

The extracellular levels of aspartate, glutamate, serine, glutamine, glycine, alanine and GABA were studied in vivo with the microdialysis technique in 15 different regions of the rat brain. The effect of high K+ on the overflow of these amino acids was also studied. These results were compared with those from a regional dissection of 17 brain regions in which the tissue content of the same amino acids was determined. The in vivo data showed an unevenly distributed KCl response of aspartate, glutamate, taurine and GABA, all of which are putative neurotransmitters. It was not possible to predict the response to high K+ from the magnitude of the unstimulated overflow. Glutamine overflow was inversely related to that of glutamate during the high K+ stimulus, which is consistent with glutamine being the main precursor of glutamate. Only for GABA and alanine was overflow proportional to the tissue level in the different regions studied.

Ethanol Potentiation of GABAergic Synaptic Transmission May Be Self-Limiting: Role of Presynaptic GABABReceptors

“…Such an effect might raise ambient GABA levels to a level sufficient to enhance presynaptic GABA B receptor function. In fact, GABA B receptors have a much lower functional EC 50 than do GABA A receptors (Sodickson and Bean, 1996), and extracellular GABA levels have been estimated to be very near the threshold that we observed for activation of presynaptic GABA B receptors at proximal GABAergic synapses (ϳ0.5-1 M) (Lerma et al, 1986;Tossman et al, 1986).…”

Effect of the GABA B agonist baclofen on dipyrone-induced delayed gastric emptying in rats

“…Different hypotheses to explain this effect have been proposed, such as the inhibition of prostaglandin production, blockade of the inactivation of adenosine (a potent inhibitory neuromodulator), activation of GABA A receptors, and an antiglutamatergic effect (32,33). Finally, an extrasynaptic presence of GABA B receptors has been proposed, although for these receptors to be activated continuously, elevated concentrations of GABA in the extracellular fluid are necessary or its concentration needs to be increased close to these receptors through the release from various neurons (4,23,34).…”

Na+-dependent Glutamate Transporters (EAAT1, EAAT2, and EAAT3) of the Blood-Brain Barrier

“…When its concentration in the extracellular fluid becomes elevated, glutamate can be toxic to neurons (1) and has been associated with serious brain damage (2). Therefore, the concentration of glutamate in the extracellular fluid is kept low (1-3 mol/liter) (3,4), even though there is 12 mol/g of whole brain (5). A possible mechanism to maintain the low concentration in the extracellular fluid has been postulated with the finding of active glutamate transport into neurons (6,7) and astrocytes (8).…”