Comparative aspects of tissue glutamine and proline metabolism.

The GDH pathway is less energy demanding than the GOGAT pathway because it does not require ATP, so it seemed possible that gdhA mutants forced to make glutamate via the more expensive pathway would not survive starvation as well as the wild type (, , , ). In order to see if gdhA mutants were impaired in recovery from starvation, I compared survival at 30°C of gdhA (RH828) and gdhA+ (RH842) strains mixed after growth in equal amounts or at a 100-fold excess of the wild type. There was no difference in survival over at least 150 days after growth in minimal glucose (0.1%) medium. Survival after growth in tryptone broth-glucose over 3 weeks gave inconsistent results. In several experiments the gdhA mutant showed lower survival, but in others it showed no significant difference from that of the gdhA+ strain. I conclude that if GDH plays a role in survival of starvation, it is a minor one under the conditions of the present study.

FIGURE 8-7 Steps involved in the synthesis and release of glutamate.

The following steps are involved in the second process of the synthesis of glutamate (Fig. 8-7).

Regulation of glutamine synthetase in Streptomyces coelicolor.

GS is a highly controlled enzyme, subject to multiple forms of regulation (, ). A cascade of regulatory proteins and small molecule effectors, primarily glutamine and 2-oxoglutarate, control synthesis of GS. Each GS monomer in the 12-member holoenzyme is subject to rapid adenylylation and deadenylylation in response to the same effectors. The adenylylated form is much less active. Partial adenylylation of the holoenzyme sensitizes it to feedback inhibition by a variety of small molecules that may be construed as end products of GS activity.

Glutamate in plants: metabolism, regulation, and signalling.

The relative importance of each of the two glutamate pathways during glucose-limited growth varies (in opposite directions) as a function of phosphate and ammonium concentrations (). However, the levels of two of the three relevant enzymes, GDH and GOGAT, remain low during glucose-limited growth in continuous culture and do not change markedly with change in ammonium or phosphate level under conditions in which pathway choice appears to be controlled by these compounds (). In the work described in this report, I looked at the level and form (adenylylated or unadenylylated) of the third enzyme, glutamine synthetase, to see if either varied with conditions controlling choice of pathway for glutamate synthesis. The results show that regulation of the form or amount of GS is also insufficient to control the choice of pathway. Thus, concentration of substrates and/or modulation of enzyme activity is likely to be a major determinant of pathway choice in glutamate synthesis.

3. In the glia, glutamate is converted into glutamine by an enzyme, glutamine synthetase.

Effect of glucose on aspartate and glutamate synthesis …

4. Glutamine is transported out of the glia into the neuro-nal terminal via glutamine transporters located in the glial and neuronal terminal membranes.

Start studying Neurotransmitters 1: Glutamate, GABA, Acetylcholine

The present study was conducted to study this metabolic interaction in cultured GABAergic neurons exposed to different combinations of (13)C-labeled and unlabeled glucose and ß-hydroxybutyrate.

► 13 C in glutamate and GABA coming from β-hydroxybutyrate exceeds that from glucose.

Glutamine metabolism and cycling in Neurospora crassa.

Glutamate metabolism in Bacillus subtilis: gene expression and enzyme activities evolved to avoid futile cycles and to allow rapid responses to perturbations of the system J.

13N isotope studies of glutamine assimilation pathways in Neurospora crassa.

The role of glutamate dehydrogenase in plant nitrogen metabolism.

4. Excitotoxic action of glutamate has been implicated in Alzheimer’s disease. One of the mechanisms of the loss of neurons concerned with memory in this disease is believed to be overexcitation and, finally, loss of these neurons by glutamate-induced activation of N-methyl-D-aspartic acid (NMDA) receptors (described later in this topic in the "Ionotropic Receptors" section). Memantine (Namenda), an NMDA receptor antagonist, is reported to mitigate this effect and slow down the symptoms of the disease.

► 13 C in glutamate and GABA coming from β-hydroxybutyrate exceeds that from glucose."

Pathway Choice in Glutamate Synthesis inEscherichia coli

The interaction between glucose and ketone bodies is complex and there is still controversy as to what extent it affects the homeostasis of the neurotransmitters glutamate, aspartate and GABA.