PubMed · 1160939
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R A Fishman. 1975-10-02. Brain edema.. https://doi.org/10.1056/nejm197510022931407
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Uptake into glial cells helps to terminate glutamate's neurotransmitter action and to keep its extracellular concentration, [Glu]o, below neurotoxic levels. The accumulative power of the uptake carrier stems from its transport of inorganic ions such as sodium (into the cell) and potassium (out of the cell). There is controversy over whether the carrier also transports a proton (or pH-changing anion). Here we show that the carrier generates an alkalinization outside and an acidification inside glial cells, and transports anions out of the cells, suggesting that there is a carrier cycle in which two Na+ accompany each glutamate anion into the cell, while one K+ and one OH- (or HCO3-) are transported out. This stoichiometry predicts a minimum [Glu]o of 0.6 microM normally (tonically activating presynaptic autoreceptors and post-synaptic NMDA receptors), and 370 microM during brain anoxia (high enough to kill neurons). Transport of OH-/HCO3- on the uptake carrier generates significant pH changes, and may provide a mechanism for neuron-glial interaction.
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We tried to use sodium acetazolamide to enhance MR angiography (MRA). Sodium acetazolamide, one of carbonic anhydrase inhibitors, has an effect to increase regional cerebral blood flow. We made a direct comparison between pre and post enhanced MRA (both 3D-TOF and 3D-PC techniques). MRA after administration of sodium acetazolamide could depict more details of cortical branches without enhancement of back-ground. So we recommend this simple method to be used widely in any examination of MR angiography.