Abstraet -In slice preparations the exchange of dissolved substances between cells and incubation mcdiiim is delayed by diffusion through the extracellular space. The delay may seriously interfere with the study of membrane transport in terms of unidirectional fluxes across the cell membranes. A three-compartment serial model has been developed to describe exchange between slice and incubat i o n medium. By aid of this model it is shown that the diffusion delay prevents determination of unidirectional fluxes for the two non-metabolizable glucose analogues 3-0-methylglueose and x-methylgliico.;idc. The membrane transport of the slowly transported 1-methylglucoside can however be examined bq aid of the model whereas the transport of 3-0-methylglucose is so rapid that it can not be ~.xamiiied with respect to V, , , K , and K , . An attempt to determine these parameters will result in falsely large wlucs which reflect extracellular diffusion and not membrane transport.

The glucose analogues 3-0-methyl-o-glucose and 1-methyl-o-glucoside were not metabolized i n brain tissue.The uptake of these two sugars into the intracellular compartment of brain cortex slices was investigated using media with normal and low Na+ concentration (replacement of all NaCl with choline CI). The cellular transport was not Na -dependent. The transport mechanism clearly distinguished between the two sugars in both normal and low Na+ media. P K I . V I~I I S studies of the uptake or iJC-labelled sugars from the perfused cerebral ventricles of cats (BWSDSTLD. 1970) and rabbits (BRADBURY & BROWSTHI. 1973) have shown that the uptake of glucose and the transport of non-metabolizable glucose analogues away from the cerebral ventricles and into surrounding tissues could be inhibited by ouabain.

Abstract— —The uptake of the glucose analogue 2‐deoxy‐d‐glucose by rat brain cortex slices was studied in order to compare the rate of membrane transport with the rate of phosphorylation in the concentration range 5–12 mM‐glucose plus 0.5–15 mM‐2‐deoxy‐glucose. The comparison was carried out by fitting a model of the brain slice to uptake data and by determination of 2‐deoxy‐glucose and 2‐deoxy‐glucose‐6‐phosphate by ion exchange chromatography. The rate of membrane transport exceeded the rate of phosphorylation by at least one order of magnitude. The membrane transport was so rapid that the extracellular diffusion became rate limiting for the uptake. The membrane transport could therefore only be determined as a minimum value and it was not possible to determine unidirectional flux across the cell membranes (initial rate). Accordingly, characterization of the membrane tranport with respect to maximal transport rate and affinity was not possible. The phosphorylation reaction, however, was so slow that it was accessible for exact determination and only the phosphorylation reaction was responsible for the fact that the cellular uptake of 2‐deoxy‐glucose was of the Michaelis‐Menten type, thus emphasizing the importance of dissociation between membrane transport and metabolism when transport is studied of a substance which can undergo metabolism. The data indicate that glucose transport across glial and neuronal membranes is not rate limiting for glucose metabolism of brain tissue in vitro.

The potassium-induced stimulation of oxygen consumption in brain slices has a threshold value of 15-20 mM potassium, and it reaches its maximum at 35-50 mM. Although this phenomenon now has been known for almost 50 years, its physiological role remains undetermined. One reason for this may be that the high concentrations of potassium that are required for this response also have many other consequences, e.g., a depolarization of the cells, and that the different effects to some extent may mask each other. For this reason this investigation studied the effects of cesium, which evokes a maximal stimulation of oxygen consumption already at 15 mM. Like potassium, concentrations of cesium that stimulate oxygen consumption also lead to an enhanced swelling. Unlike potassium, the sodium content is affected very little by these concentrations of cesium, whereas cesium and chloride contents are increased. On this basis it is concluded that the cesium-induced stimulation of oxygen uptake is a metabolic manifestation of an active uptake of cesium and chloride, which secondarily leads to an uptake of water, i.e., the cesium-induced swelling. Analogously, it is suggested that the potassium-induced stimulation of oxygen uptake represents an active accumulation of potassium and chloride.

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