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At Healthfully, we strive to deliver objective content that is accurate and up-to-date. Our team periodically reviews articles in order to ensure content quality. The sources cited below consist of evidence from peer-reviewed journals, prominent medical organizations, academic associations, and government data.
- MayoClinic.com; Depression; February 2010
- National Institute of Mental Health; Brain Basics; June 2011
- "CNS and Neurological Disorders Drug Targets"; Metabotropic Glutamate Receptors in the Control of Mood Disorders; Jeffrey M. Witkin, et al.; April 2007
- "CNS and Neurological Disorders Drug Targets"; Metabotropic Glutamate Receptors in the Control of Mood Disorders; Jeffrey M. Witkin, et al.; April 2007
- "The American Journal of Psychiatry"; An Open-Label Trial of Riluzole in Patients With Treatment-Resistant Major Depression; Carlos A. Zarate, et al.; January 2004
- "The American Journal of Psychiatry"; An Open-Label Trial of Riluzole in Patients With Treatment-Resistant Major Depression; Carlos A. Zarate, et al.; January 2004
The information contained on this site is for informational purposes only, and should not be used as a substitute for the advice of a professional health care provider. Please check with the appropriate physician regarding health questions and concerns. Although we strive to deliver accurate and up-to-date information, no guarantee to that effect is made.
Glutamate & Depression
Glutamate, serotonin and norepinephrin are neurotransmitters, substances that conduct signals from one nerve cell to another. Depression and other mental illnesses can arise if this signalling process goes awry. Standard drug therapies for depression have included selective serotonin reuptake inhibitors, such as fluoxetine, and drugs such as duloxetine, a serotonin and norepinephrin reuptake inhibitor. Experimental drugs that block glutamate receptors in the central nervous system or lower glutamate brain levels may represent the next generation of antidepressant medications, and offer potential advantages over current drug treatments.
If you are experiencing serious medical symptoms, seek emergency treatment immediately.
Depression
Depression is a mental illness that usually requires prolonged treatment with medication, psychological counseling, residential treatment programs or other therapies depending on the severity of the condition. Scientists think depression stems from factors that include heredity, brain levels of certain neurotransmitters, hormonal changes, personal tragedies such as:
- the loss of a loved one,
- early childhood trauma
According to MayoClinic.com, risk factors for depression include having relatives diagnosed with the condition or relatives who committed suicide, having low self esteem or excessive dependence on someone else, experiencing traumatic events in childhood, having a serious health condition such as cancer or heart disease, being poor, or abusing alcohol or illegal drugs 1. Symptoms include
- feeling sad or unhappy
- loss of interest in everyday activities
- excessive sleeping
- changes in appetite
- agitation
- decreased concentration
- loss of energy
- feelings of worthlessness or guilt
Role of Glutamate
St John's Wort & Food Interactions
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Glutamate is the most abundant excitatory neurotransmitter. According to the National Institute of Mental Health, excitatory neurotransmitters are those that promote the flow of signals between nerve cells, thereby supporting the proper functioning of the cells. Scientists think glutamate may play a part in the learning process, and it may also help with memory. Mental disorders such as depression and schizophrenia stem in part from an inability of the central nervous system to effectively use glutamate.
- Glutamate is the most abundant excitatory neurotransmitter.
- Mental disorders such as depression and schizophrenia stem in part from an inability of the central nervous system to effectively use glutamate.
Glutamate Receptor Blockers
Glutamate receptors are molecular structures situated on the surface of nerve cells. These structures selectively bind to glutamate, and this binding regulates glutamate-mediated nerve signals and the body's response to these signals. ; April 2007'). Such compounds offer the possibility of treating depression through a novel mechanism of drug action.
- Glutamate receptors are molecular structures situated on the surface of nerve cells.
Glutamate Brain Levels
Role of Serotonin in Anxiety
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; December 2007')5. This finding implies that elevated glutamate brain levels may be one of the causative factors in depression. The experimental drug riluzole increases glutamate uptake and curtails its release, thereby lowering glutamate brain levels. In a clinical study reported in the January 2004 issue of "The American Journal of Psychiatry," researchers found that riluzole markedly improved the major depression symptoms of all 19 study subjects 5.
Related Articles
References
- MayoClinic.com; Depression; February 2010
- "CNS and Neurological Disorders Drug Targets"; Metabotropic Glutamate Receptors in the Control of Mood Disorders; Jeffrey M. Witkin, et al.; April 2007
- "Biological Psychiatry"; Increased Levels of Glutamate in Brains From Patients With Mood Disorders; Kenji Hashimoto, et al.; December 2007
- PsychCentral.com; Lou Gehrig's ALS Medication Riluzole For Bipolar Depression; Candida Fink; March 2011
- "The American Journal of Psychiatry"; An Open-Label Trial of Riluzole in Patients With Treatment-Resistant Major Depression; Carlos A. Zarate, et al.; January 2004
- Hannestad U, Theodorsson E, Evengård B. beta-Alanine and gamma-aminobutyric acid in chronic fatigue syndrome. International journal of clinical chemisty. 2007 Feb;376(1-2):23-9.
- Harris RE, et. al. Elevated insular glutamate in fibromyalgia is associated with experimental pain. Arthritis and rheumatism. 2009 Oct;60(10):3146-52.
- Kuratsune H, Yamaguti K, Lindh G, et al. Brain regions involved in fatigue sensation: reduced acetylcarnitine uptake into the brain. NeuroImage. 2002 Nov;17(3):1256-65.
- Martins DF, Siteneski A, Ludtke DD, et al. High-intensity swimming exercise decreases glutamate-induced nociception by activation of g-protein-coupled receptors inhibiting phosphorylated protein kinase a. Molecular neurobiology. 2016 Sep 13. [Epub ahead of print]
- Smith AK, Fang H, Whistler T, et al. Convergent genomic studies identify association of GRIK2 and NPAS2 with chronic fatigue syndrome. Neuropsychobiology. 2011;64(4):183-94.
Writer Bio
Robert DiPardo has been a pharmaceutical chemist for more than 30 years. He has co-authored several scientific publications on cardiovascular disease, osteoarthritis, Alzheimer's disease and other therapeutic areas. DiPardo retired from drug discovery research in 2009 and, since 2010, has covered fitness and well-being for various online publications. DiPardo holds a Master of Science in organic chemistry from Yale University.