Read e-book online Advances in Neurochemistry PDF

By Louis Sokoloff (auth.), B. W. Agranoff, M. H. Aprison (eds.)

This sequence has been directed at supplying scientists owning significant bio­ chemical historical past with really expert studies of neurobiological curiosity. a few have handled accomplished our bodies of study, whereas others encompass broad experiences of study in growth, judged to be of present curiosity to the lively researcher. we've chosen well-known scientists and allowed them freedom to mirror and speculate within the box within which they've got accomplished promenade­ inence. We word with unhappiness the passing of Dr. 10rdi FoIch-Pi, who served as an advisory editor whilst the sequence was once initiated. He performed a relevant function within the improvement of neurochemistry, in addition to the production societies and journals. he'll be remembered fondly by means of all these whose lives he touched. The editors recognize the cooperation of the Upjohn corporation within the guidance of the colour plate incorporated during this quantity. We additionally recognize the skillful editorial assistance of Dr. Kenneth C. Leskawa. we're happy to honor the retirement of Dr. E. Martin Gal, a former advisory editor of Advances, with the inclusion of a bankruptcy by way of him during this volume.

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The trapping of [14C]-DG-6-P has recently been questioned by Hawkins and Miller (1978), who presented what they considered to be evidence of significant loss of [14C]-DG-6-P under the conditions specified by the [14C]-DG method. First, they cited a number of references in the literature that have reported higher levels of glucose-6-phosphatase activity than were observed by Hers and DeDuve (1950) and Hers (1957). 5 in the presence of deoxycholate, which activates this normally enzyme-bound enzyme.

Furthermore, these determinant factors are likely to be different for each structure of the brain. To minimize the problem of loss of 14C02, it is necessary to keep the experimental period very short before there has been significant formation and 42 CHAPTER 1 loss of 14C02. This, however, introduces another equally complex problem. The rate of formation of labeled product depends not only on the rate of the chemical reaction but also on the specific activity of the precursor pool. In the intact animal it is impossible to measure the time courses of the specific activity of the glucose pool in all the structures of the brain.

Varies with the blood flow, blood-brain barrier transport, and plasma glucose level. These are all functions that may vary from structure to structure within the brain, from animal to animal, and from condition to condition. The single set of rate constants in Table 1 was determined in normal conscious rats and cannot possibly be accurate for all conditions. The influence of inaccuracies in the rate constants is minimized, however, by the design of the procedure adopted for the measurement of local cerebral glucose utilization, namely, the use of an intravenous pulse of [14C]-DG at zero time followed by a long interval of time before killing.

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