Recent advances in quantitative microanalysis (Edstr6m, 1953, 1960) have permitted measurement of change in ribonucleic acid (RNA) content of individual neurones after cutting their axons (Brattgard, Edstr6m & Hyden, 1957). As measurement of a cell's content of RNA alone can give little indication of its dynamic intracellular turnover, the present investigation was undertaken with tritium (3H) labelled precursors of RNA. Their incorporation into various subcellular compartments was detected autoradiographically. The investigation also includes a study of deoxyribonucleic acid (DNA) synthesis within perineuronal oligodendroglia.

An autoradiographic study of the incorporation of nucleic‐acid precursors by neurones and glia during nerve stimulation.

Publisher Summary This chapter provides an overview of purines and pyrimidines and their biosynthesis. The pathways of purine and pyrimidine metabolism have been greatly aided by tracer research, nutritional and genetic studies with intact organisms, and tissue studies in vitro. The study of purine synthetic reactions was complicated by the increased formation of purine bases from the breakdown of tissue nucleic acids and nucleotides upon homogenization of the tissue. The utilization of free purines is accomplished by reaction with PRPP to form nucleotides directly. The bases have also been converted to nucleotides via the nucleosides. Nucleosides are produced by reaction of free bases with ribose 1-phosphate in the presence of nucleoside phosphorylase. The extensive utilization of dietary adenine and the nonutilization of guanine in rat have been explained in terms of the relative absence of the enzyme adenase and the presence of much guanase in rat tissues. The synthesis of purines de novo was initiated by the formation of 5-phosphoribosylamine by reaction of glutamine with 5-phosphoribosylpyrophosphate. The nucleotides that are constituents of nucleic acids, namely, guanylic acid and adenylic acid, were formed from inosinic acid.

Purines and Pyrimidines

https://www.cell.com/trends/pharmacological-sciences/pdf/S0165-6147(99)01298-5.pdf

Uridine and its nucleotides: biological actions, therapeutic potentials.

BETZ, A. LORRIS, DAVID D. GILBOE, DAVID L. YUDILEVICH, AND LESTER R. DREWES. Kinefics of unidz’rechzal glucose fransport into the isoluted dog brain. Am. J. Physiol. 225(3): 586592* 1973.An indicator-dilution technique with 22Na as the intravascular marker was used to measure unidirectional transport of D-glucose6-3H from blood into the isolated dog brain. The rate of unidirectional glucose transport, v, was calculated from the equation v = (E 0.036) A Fp/W, where E is the fractional extraction of glucose from the blood, A is the arterial plasma glucose concentration, Fp/W is the plasma flow rate per unit weight of brain, and 0.036 is a correction for glucose diffusion. The diffusion correction was based on the fractional extraction of D-fructose-6-“H, a hexose that is not transported into brain. The results of experiments in which Fp/W was varied while A was held constant indicate that an increased flow rate results in an increased rate of glucose uptake. Because of the Aow effect, the kinetics of unidirectional glucose transport were studied in six brains in which Fp/W was held constant while A was varied between 4.3 and 60 mM. An apparent Kna for glucose transport of 8.26 =t 1.67 mM and a Vmax of 1.75 + .I 1 pmoles/g of brain per minute were calculated. The kinetics were not significantly altered in the presence of pentobarbital (25 mg/liter) or insulin (4 pg/lOO ml), This technique is generally applicable to any isolated, perfused tissue.

Kinetics of unidirectional glucose transport into the isolated dog brain

Changes in the Blood-Brain Barrier in Hepatic Coma After Hepatectomy in the Rat

THE nutritional requirements of the brain were investigated previously in perfusion experiments on cats. It has been shown that the carbohydrate metabolism of the brain, and its survival, is dependent on substances which are produced or released by the liver into the blood circulation. In the absence of the liver, aerobic glycolysis developed in the brain, followed later by impermeability to glucose, reducing the survival time of the perfused brain to about one hour. Insertion of the liver into the circulation corrected the faulty carbohydrate metabolism of the brain and prolonged its survival by several hours. (GEIGER, MAGNFS, TAYJ,OR, and VFXALLI, 1954). It was found in the present experiments that, by adding small amounts of cytidine and uridme to the perfusion fluid, it was possible to maintain the perfused brain in good functional condition with a normal carbohydrate metabolism for four hours or longer without the liver. These experiments indicate the necessity of these nucleosides for the maintenance of normal brain functions and metabolism. An attempt is also made to elucidate the mechanism of action of these substances on brain metabolism.

S Yamasaki

Papers

Cytidine and uridine requirement of the brain.