Hostname: page-component-586b7cd67f-gb8f7 Total loading time: 0 Render date: 2024-11-22T13:25:49.657Z Has data issue: false hasContentIssue false
  • English
  • Français

A Note on the Ammonia and Glutamine Content of the Cerebrospinal Fluid

Published online by Cambridge University Press:  08 February 2018

D. Richter ,
R.M.C. Dawson  and
Linford Rees
D. Richter
Affiliation:
Neuropsychiatric Research Centre, Whitchurch Hospital, Cardiff
R.M.C. Dawson
Affiliation:
Neuropsychiatric Research Centre, Whitchurch Hospital, Cardiff
Linford Rees
Affiliation:
Neuropsychiatric Research Centre, Whitchurch Hospital, Cardiff
Get access Rights & Permissions [Opens in a new window]

Extract

Tashiro (1922) showed that the isolated frog nerve liberates ammonia on stimulation, and Richter and Dawson (1948) have recently found that ammonia is liberated on stimulation by the brain. Ammonia is very toxic to the brain, on which it has an irritant action; but the brain may be protected to some extent by the enzyme system described by Krebs (1935), which can detoxicate ammonia by combination with glutamic acid to form glutamine. Sapirstein (1943) obtained evidence that this system is active in vivo by showing that glutamic acid increases the resistance of animals to convulsions produced by injecting ammonium chloride. The toxic action of ammonia on the brain is also of interest in connection with the view that it may be concerned in certain forms of epilepsy (Harris, 1945). This view is supported by the observations of Price, Waelsch and Putnam (1943) on the inhibitory action of glutamic acid on petit mal attacks.

Type
Part I.—Original Articles
Information
Journal of Mental Science , Volume 95 , Issue 398 , January 1949 , pp. 148 - 152
Copyright
Copyright © Royal College of Psychiatrists, 1949 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Brühd, H. H. (1938), Z. Kinderheilk., 59, 446.Google Scholar
Conway, E. J. (1939), Micro-Diffusion Analysis and Volumetric Error. London.Google Scholar
Harris, M. M. (1943), J. clin. Invest., 22, 569.Google Scholar
Harris, M. M. (1945), J. Nerv. Ment. Dis., 102, 466.Google Scholar
Krebs, H. A. (1935), Biochem. J., 29, 1951.CrossRefGoogle Scholar
Price, J. C., Waelsch, H., and Putnam, T. J. (1943), J. Amer. Med. Ass., 122, 1153.CrossRefGoogle Scholar
Richter, D., and Dawson, R. M. C. (1948), J. Biol. Chem., in the press.Google Scholar
Riebeling, C. (1930), Z. ges. Neurol. Psychiat., 128, 475.Google Scholar
Sapirsteim, M. R. (1943), Proc. Soc. Exp. Biol., N.Y., 52, 334.Google Scholar
Tashiro, S. (1922), Amer. J. Physiol., 60, 519.Google Scholar
Tietz, E. B., Thompson, G. N., van Harreveld, A., and Wiersma, C. A. G., J. Nerv. Ment. Dis., 103, 144.CrossRefGoogle Scholar
Submit a response

eLetters

No eLetters have been published for this article.