468 H. H. TALLAN 
In assessing the effects of the drugs we have studied on glutamic acid, glutamine, 
and glutathione, the variation between animals in the same group prevents the 
assignment of any clear-cut action. OkUMURA e¢ al.” do report increases in the three 
compounds after the administration of chlorpromazine. In mice, brain glutamic 
acid is unaffected by reserpine’. The reported actions of other psychotropic drugs 
on these substances may be noted here. The concentration of glutamic acid has been 
found to be unaffected by many convulsive agents*: % 11, 14, 16, 21 and by metham- 
phetamine?; to be decreased by other convulsants®: !° and in epileptogenic lesions!’, 
as well as by the anticonvulsant diphenylhydantoin”?, the tranquilizer mepro- 
bamate?? and the anesthetic thiopentone*4; and to be increased by ethanol” and 
KCN (ref. 13). The concentration of glutamine is reported to be unaffected by 
some convulsants?!® 26, by ethanol?®, and by nembutal®®; to be decreased in cortical 
areas subjected to epileptogenic lesions!” ; and to be increased by an anticonvulsant”? 
and a convulsant?®, in thiopentone anesthesia*4, and in ammonium poisoning® (cf. 
ref. 4). The concentration of glutathione has been found to be decreased by a pyri- 
doxine antagonist? and in pyridoxine deficiency?’, and to be lowered in cortical 
areas subjected to epileptogenic lesions!’. A common ground for these diverse actions 
is not readily apparent; the primary effect of these psychotropic agents is almost 
certainly not on the amino acids of the brain. 
Ethanolamine and its derivatives are compounds that have received relatively 
little attention. Within the present series, definite elevations occur in the concen- 
tration of glycerophosphoethanolamine (GPE) after imipramine and reserpine. The 
possibility that an increase in GPE may be the result of post mortem breakdown 
of phosphatidylethanolamine (cf. ANSELL AND NORMAN?S) must be considered, but 
is unlikely since all of the brain extracts were prepared in precisely the same way; 
whether the concentration of phosphatidylethanolamine itself had been increased 
was not investigated. OKUMURA e¢ al.? found a decrease in GPE after chlorpromazine, 
not observed in the present work, as well as a decrease after fasting or the administra- 
tion of insulin or methamphetamine. There is no clear-cut change in the present 
series in either phosphoethanolamine (PE) or ethanolamine. ANSELL AND SPANNER?® 
found that insulin decreased the synthesis of brain PE without affecting the actual 
amount present, and OkumuRA e¢ al.” found an increase in PE after fasting and after 
methamphetamine administration. 
Acetylaspartic acid is of great interest in that it occurs normally only in brain*®, 
though Du RuissEAu*! has shown that large amounts are found in the liver of animals 
poisoned with ammonium acetate, which, however, has no effect on the brain acetyl- 
aspartic acid*!. OkuMuRA et al. report an appreciable increase after administration 
of methamphetamine. Marcotis ef al.°?. found no change in nembutal narcosis; 
their data suggest a lowering after metrazole-induced convulsions. In the present 
work, there is a slight decrease after chlorpromazine (not seen, however, by OKUMURA 
et al.*), and perhaps after desmethyl-imipramine. Aspartic acid itself is unaffected 
by the drugs used in the present study. It is reported that no change in aspartic acid 
occurs following reserpine®, various convulsants®: ". 16, 32, and imino- f, /’-dipropio- 
nitrile**; there is a decrease after nembutal®? or ammonium acetate*, an increase 
after ethanol*® or insulin (cf. ref. 2). 
Taurine is of interest because, as has been found by Hope*‘, the concentration 
in brain is not affected by extreme pyridoxine deficiency, although the urinary 
References p. 469/470 
