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Comment
. 2010 Nov 1;68(9):780-2.
doi: 10.1016/j.biopsych.2010.09.011.

Magnetic resonance spectroscopy studies of the glutamatergic system in mood disorders: a pathway to diagnosis, novel therapeutics, and personalized medicine?

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Comment

Magnetic resonance spectroscopy studies of the glutamatergic system in mood disorders: a pathway to diagnosis, novel therapeutics, and personalized medicine?

Giacomo Salvadore et al. Biol Psychiatry. .
No abstract available

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Conflict of interest statement

Dr. Zarate is listed as a co-inventor on a patent for the use of ketamine in major depression. Dr. Zarate has assigned his patent rights on ketamine to the US government. Dr. Salvadore reports no biomedical financial interests or potential conflicts of interest.

Figures

Figure 1
Figure 1
The tripartite glutamatergic system and magnetic resonance spectroscopy studies in mood disorders. The glutamate (Glu)-glutamine (Gln) cycle plays a key role in the regulation of presynaptic and postsynaptic ionic and metabotropic glutamate receptors that have been implicated in the pathophysiology of mood disorders. In the brain, glutamate can either be synthesized de novo from glucose via the Krebs cycle and the transamination of α-oxoglutatrate or it can be recycled through the Glu/Gln cycle (see above). Glutamate is transported into synaptic vesicles by vesicular Glu transporters. Once released, Glu binds to and activates ionotropic and metabotropic receptors found throughout the central nervous system that have wide-ranging effects on neural excitability. There are three excitatory ionotropic receptors identified by their pharmacological properties as AMPA, kainate, and NMDA receptors. Metabotropic glutamate receptors couple to different signal transduction systems and ligand sensitivities. Glutamate is cleared from the extracellular space via high-affinity excitatory amino acid transporters in neighboring glial cells, which convert Glu into Gln via the action of glutamine synthetase. Glutamine is then transported back into the glutamatergic neuron where it is hydrolyzed by glutaminase back into Glu. AMPA, α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid; BPD, bipolar disorder; 13C MRS, carbon-13 magnetic resonance spectroscopy; EAAT, excitatory amino acid transporter; Glx, glutamine plus glutamate; MDD, major depressive disorder; mGluR2/3, metabotropic glutamatergic receptor 2 and 3; NMDA, N-methyl-D-aspartate; NR2A, NMDA receptor sybtype 2A; NR2B, NMDA receptor subtype 2B; PSD, postsynaptic density; VLGUT, vesicular Glu transporters.

Comment on

References

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