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EFFECTS OF EXCITATION AND ANAESTHESIA ON THE GLUTAMINE CONTENT OF THE RAT BRAIN WITH A REFERENCE TO THE ADMINISTRATION OF GLUTAMINE
Author(s) -
Dobkin J.
Publication year - 1972
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1972.tb01440.x
Subject(s) - glutamine , convulsant , saline , anesthesia , pentylenetetrazol , chemistry , glutamate receptor , medicine , endocrinology , pharmacology , biochemistry , amino acid , anticonvulsant , receptor , psychiatry , epilepsy
— A study of the factors affecting the ghtamine content in brain of rats showed that it was significantly decreased by intraperitoneal injection of physiological saline and by the stimulus of decapitation. It fell markedly at the stage of delirium (excitement) of pentobarbitone sodium anaesthesia and returned to the original value in light and deep surgical anaesthesia; after pentylenetetrazol injection the glutamine content showed a tendency to decrease but this change was only significant in relation to its post‐saline level when the convulsant and 0.9 % NaCl were given to lightly‐anaesthetized animals. The i.p. administration of glutamine temporarily abolished the decrease in its concentration in the brain caused by injection and decapitation but never raised it above the original level. Many rats previously treated with glutamine showed no signs of excitement during the induction period of pentobarbitone sodium anaesthesia, and those which were excited showed a comparatively smaller decrease of brain glutamine content. whereas in the anaesthetic state there was no change in the content of brain glutamine after glutamine had been administered. Pentylenetetrazol given at the dose level of 200 mg/kg, but not at that of 100 mg/kg, resulted in the uptake of the added glutamine by the brain up to its normal concentration. Hence, the added glutamine did not readily enter normal or anaesthetized brain, but did penetrate the hyperactive brain where its level had fallen. The brain levels of free glutamic and aspartic acids were not affected, in general, by procedures which increased cerebral activity. Glutamate was decreased by deep anaesthesia, whereas aspartate was not significantly altered in any of the conditions which were tested. The significance of these results in relation to cerebral ammonia metabolism and possible changes of the permeability of the tissue to glutamine in different functional states is discussed.