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Journal ArticleDOI

Water distribution in incubated slices of brain and other tissues.

01 Sep 1956-Biochemistry and Cell Biology (NRC Research Press Ottawa, Canada)-Vol. 34, Iss: 5, pp 1007-1022
TL;DR: With glutamate or high potassium in the medium, swelling is increased and the non-thiocyanate, non-sucrose, and non-inulin spaces increase correspondingly, and this increase is apparently intracellular.
Abstract: Slices of rat cerebral cortex swell about 40% during one hour's aerobic incubation in bicarbonate-buffered medium. Thiocyanate or sucrose added to the medium equilibrate with part of the tissue flu...
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TL;DR: Evidence was obtained that so-called small granular vesicles are characteristic of central and peripheral monoamine neurons, and that these vesicle represent the main storage sites of the monoamines.
Abstract: Using ice-cold 3% potassium permanganate as a fixative (Richardson, 1966), isolated tissues from the central and peripheral nervous system were investigated in the electron microscope, with the object of identifying monoamine-containing neurons at the ultrastructural level. Thin brain slices and peripheral tissues from untreated rats and from rats treated with drugs interfering with monoamine metabolism (e.g. reserpine, H 44/68 or tetrabenazine) were incubated in physiological buffer solutions without and with monoamines in different concentrations. In certain cases, drugs interfering with monoamine metabolism (e.g. amphetamine, desipramine, cocaine or phenoxybenzamine) in different concentrations were added to the incubation medium.

468 citations

Journal ArticleDOI
TL;DR: Since the first electron microscope observations on sections of the central nervous system, it has been found that the glial elements fill all intervening spaces between the neurons and the vascular elements and that no real extracellular spaces are present within thecentral nervous system.
Abstract: STRUCTURAL ANALYSIS of the central nervous system with so-called selective histologic technics is hindered by the fact that only partial views of the total organization are obtained. Thus the methods for the demonstration of astroglia, oligodendroglia, microglia, myelin sheaths, Nissl substance, and so forth emphasize only one component at a time and do not permit a spatial integration of all structural elements. On the contrary, with the electron microscope, all these and other components can be visualized simultaneously in thin sections fixed in osmium tetroxide and can be followed in their topographic relationships down to dimensions beyond the resolving power of the optical microscope. With this technic, the different types of glial cells that exist in the central nervous system may be recognized bv their morphology, and their relationships with neurons, nerve fibers and endings, and so forth can be clearly determined.'\" Since the first electron microscope observations on sections of the central nervous system, it has been found that the glial elements fill all intervening spaces between the neurons and the vascular elements and that no real extracellular spaces are present within the central nervous system.+8 The plasma membranes of all cellular components of the nervous tissue are in intimate contact with themselves and with the basal membranes of the capillaries. A distance of only 120 to 250 A can be observed between the adjacent membranes, and this is filled by a material of definite electron density.9 These facts completely contradict many physiologic observations that indicate the existence of a definite extracellular space in the central nervous system.10

208 citations

Journal ArticleDOI
TL;DR: Electrophysiological evidence indicates that hyposmolality promotes epileptiform activity by strengthening both excitatory synaptic communication in neocortex and field effects among the entire cortical population, and little evidence that associated hyponatremia in itself leads to increased CNS excitability helps in understanding how rapid lowering of plasma osmolality in clinical situations can promote the hyperexcitability associated with generalized tonic-clonic seizure.

173 citations

Journal ArticleDOI
TL;DR: During evaluations of its toxicity in animals preliminary to trials, LANDAU and LUBS (1958) observed neurological signs and symptoms which closely resembled those of insulin-induced hypoglycaemia, resulting in a situation of simultaneous hyperglycaemia and cytoglycopenia.
Abstract: PREVIOUS iiivestigations have characterized 2-deoxy-~-glucose* as an inhibitor of glucose metabolism. Its effectiveness in inhibiting glycolysis and growth of neoplastic tissues (ELY, 1954; WOODWARD and HUDSON, 1954; SOKOLOFF et al., 1956; BALL, WICK and SANDERS, 1957) suggested clinical applications. During evaluations of its toxicity in animals preliminary to such trials, LANDAU and LUBS (1958) observed neurological signs and symptoms which closely resembled those of insulin-induced hypoglycaemia. After oral or parenteral administration, 2-deoxyglucose is rapidly distributed throughout the body and appears promptly in the cerebrospinal fluid (WICK, DRURY and MORITA, 1955; LANDAU and LUBS, 1958). Using doses of the order of 12 m-moles/kg, LANDAU and LUBS (1958) found an elevation of blood glucose to levels two or three times normal control values. Under such conditions both blood glucose and 2-deoxyglucose respond to insulin (WICK et al., 1955), but the insulin-mediated decrease in blood glucose to normal ranges intensifies the apparent hypoglycaemic picture. These observations are consistent with inhibition of tissue utilization of glucose in the presence of 2-deoxyglucose, resulting in a situation of simultaneous hyperglycaemia and cytoglycopenia, which in the central nervous system is expressed as dysfunctions usually associated with hypoglycaemia. 2-Deoxyglucose is readily phosphorylated by yeast, muscle and brain hexokindse (SOLS and CRANE, 1954; WOODWARD and HUDSON, 1955; WICK et al., 1957), and it produces inhibition of glycolysis in yeast and various mammalian tissues, including brain (WOODWARD, 1952; WOODWARD and HUDSON, 1954). Metabolism of 2deoxyglucose-6-phosphate appears not to occur (SOLS and CRANE, 1954; WICK et al., 1957) and in purified kidney preparations it has been reported to block conversion of glucose-6-phosphate to fructose-6-phosphate, with possible secondary effects on hexokinase (WICK et al., 1957). Few studies of the effects of 2-deoxyglucose on cerebral metabolism have been reported. Anaerobic glycolysis of rat cerebral cortex slices is inhibited 50 per cent when incubated with 1 m~-2-deoxyglucose plus 15 mwglucose in vitro, a result comparable to those obtained with rat diaphragm or with tumour tissues under similar conditions, but oxygen uptake by rat cerebral cortex appears much less

158 citations

Journal ArticleDOI
TL;DR: Arachidonic acid, at concentrations of 0.015 and 0.03 μmol/mg protein, significantly inhibited glutamate uptake in neurons, whereas 20 times higher concentrations were required for astrocytes, and the inhibitory effect was observed within 10 min of incubation with arachidic acid.
Abstract: The effects of arachidonic acid on glutamate and gamma-aminobutyric acid (GABA) uptake were studied in primary cultures of astrocytes and neurons prepared from rat cerebral cortex. The uptake rates of glutamate and GABA in astrocytic cultures were 10.4 nmol/mg protein/min and 0.125 nmol/mg protein/min, respectively. The uptake rates of glutamate and GABA in neuronal cultures were 3.37 nmol/mg protein/min and 1.53 nmol/mg protein/min. Arachidonic acid inhibited glutamate uptake in both astrocytes and neurons. The inhibitory effect was observed within 10 min of incubation with arachidonic acid and reached approximately 80% within 120 min in both types of culture. The arachidonic acid effect was not only time-dependent, but also dose-related. Arachidonic acid, at concentrations of 0.015 and 0.03 mumol/mg protein, significantly inhibited glutamate uptake in neurons, whereas 20 times higher concentrations were required for astrocytes. The effects of arachidonic acid were not as deleterious on GABA uptake as on glutamate uptake in both astrocytes and neurons. In astrocytes, GABA uptake was not affected by any of the doses of arachidonic acid studied (0.015-0.6 mumol/mg protein). In neuronal cultures, GABA uptake was inhibited, but not to the same degree observed with glutamate uptake. Lower doses of arachidonic acid (0.03 and 0.015 mumol/mg protein) did not affect neuronal GABA uptake. Other polyunsaturated fatty acids, such as docosahexaenoic acid, affected amino acid uptake in a manner similar to arachidonic acid in both astrocytes and neurons. However, saturated fatty acids, such as palmitic acid, exerted no such effect. The significance of the arachidonic acid-induced inhibition of neurotransmitter uptake in cultured brain cells in various pathological states is discussed.

151 citations