The time course of metabolism of (U-\sp?C) glutamate and (1-\sp?C) GABA by young transpiring wild type and transgenic tobacco (Nicotiana tabacum L. cv. Samsun. NN) shoots overexpressing glutamate decarboxylase was examined in the presence of the glycine decarboxylase inhibitor aminoacetonitrile. When the recycling of photorespiratory ammonium and the metabolism of (U-\sp?C) glutamate via GS/GOGAT was prevented by aminoacetonitrile, the size of the glycine and 2-oxoglutarate pools, respectively, increased to 300% and 1000-2800% of the controls after two hours, whereas the pool size and \sp?C-content of glutamine decreased to 60% and 30% of the controls, respectively. The proportion of \sp?C in Krebs-cycle organic acids increased from 10-25% to 30-40% of the controls. Succinate was labeled to a greater extent than citrate/2-oxoglutarate at the earliest sampling time of 15 min. The data were interpreted as support for an increased flux of carbon through the GABA shunt when glutamine metabolism was inhibited. I propose that under nitrogen limitation, glutamate metabolism via the GABA shunt is a mechanism to maintain the carbon:nitrogen balance in the plant.