Abstract
The results presented here indicate that glutamine in cerebrospinal fluid is likely to be making an essential contribution in vioo as a substrate for nerve-endings, as well as to other compartments. The high activity of glutaminase in synaptosomes and their lack of formation of glutamine emphasize the possible importance of glutamine as a nitrogen and carbon source for the nerve-ending. This has already been indicated from theoretical schemes (BalBzs et a!., 1973; Van den Berg & Garfinkel, 1971) and suggests that glutamine should be included in incubation fluids as a standard component. The inhibitory effect of NH4+ on glutaminase activity indicates the likely mode of action of this ion in producing raised glutamine concentrations in brain and cerebrospinal fluid during hepatic encephalopathy and after portocaval anastomosis. Coma, which does not occur in the rat at these low blood NH4+ concentrations, could occur in other more susceptible animals such as dog, or in man, as the result of a diminution of the pools of the excitatory transmitter amino acids glutamate and aspartate if the utilization of glutamine from cerebrospinal fluid were sufficiently diminished in the nerve-terminal.
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