Journal
MOLECULAR PSYCHIATRY
Volume 7, Issue -, Pages S71-S80Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.mp.4001021
Keywords
N-methyl-D-aspartate (NMDA); depression; bipolar disorder; magnetic resonance spectroscopy; anticonvulsant; voltage-gated calcium channel; metabotropic glutamate receptor; serotonin-2A receptor; premenstrual dysphoric disorder; panic disorder
Funding
- NIMH NIH HHS [K23 MH001830] Funding Source: Medline
- NATIONAL INSTITUTE OF MENTAL HEALTH [K23MH001830] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Glutamate and gamma-amino butyric acid (GABA) systems are emerging as targets for development of medications for mood disorders. There is increasing preclinical and clinical evidence that antidepressant drugs directly or indirectly reduce N-methyl-D-aspartate glutamate receptor function. Drugs that reduce glutamatergic activity or glutamate receptor-related signal transduction may also have antimanic effects. Recent studies employing magnetic resonance spectroscopy also suggest that unipolar, but not bipolar, depression is associated with reductions in cortical GABA levels. Antidepressant and mood-stabilizing treatments also appear to raise cortical GABA levels and to ameliorate GABA deficits in patients with mood disorders. The preponderance of available evidence suggests that glutamatergic and GABAergic modulation may be an important property of available antidepressant and mood-stabilizing agents. Future research will be needed to develop and evaluate new agents with specific glutamate and GABA receptor targets in the treatment of mood disorders.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available