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Statins, pain, glutamate (relates to leg pain post caffeine?)
The McMaster research team found muscle cells treated with statins released the amino acid called glutamate at much higher levels than muscle cells that were untreated. As glutamate is a potent activator of muscle pain receptors, this release was proposed to trigger the sensation of muscle pain.
Thomas Hawke, senior author of the study and a professor in pathology and molecular medicine at McMaster University said: "We found that statins were able to enter the muscle cells and cause oxidative stress. This resulted in the muscle trying to increase its production of antioxidants to combat this stress. The side-effect of this antioxidant production was the release of glutamate out of the muscle cells."
Broccoli sprout compound may restore brain chemistry imbalance linked to schizophrenia -- ScienceDaily
They say the results advance the hope that supplementing with broccoli sprout extract, which contains high levels of the chemical sulforaphane, may someday provide a way to lower the doses of traditional antipsychotic medicines needed to manage schizophrenia symptoms, thus reducing unwanted side effects of the medicines.
"It's possible that future studies could show sulforaphane to be a safe supplement to give people at risk of developing schizophrenia as a way to prevent, delay or blunt the onset of symptoms," adds Akira Sawa, M.D., Ph.D., professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine and director of the Johns Hopkins Schizophrenia Center.
Lack of a Single Molecule May Indicate Severe and Treatment Resistant Depression - Neuroscience News
Naturally produced by the body, LAC performs a number of crucial tasks in the brain. For example, the molecule regulates energy metabolism and interacts with DNA to promote the expression of important genes. Specifically, it acts on a gene that controls levels of the neurotransmitter glutamate–a chemical implicated in almost everything that the brain does.
McEwen, the Alfred E. Mirsky Professor, and Nasca, a postdoctoral fellow of the American Foundation for Suicide Prevention, have studied the link between LAC and mood disorders using animal models. In one study, they showed that LAC supplements ameliorate depressive symptoms in mice by reversing brain-cell impairment caused by an excess of glutamate. In a separate rodent study, they observed that LAC treatment reduces depressive behavior and stress-associated neural dysfunction in the medial amygdala, a brain region involved in social interactions. These findings strongly suggest that LAC deficits contribute to a depression-like state in mice, leading the scientists to wonder whether the molecule plays a similar role in humans.
Suicide is a national epidemic. We need to treat it like one. - The Washington Post
These two treatments are obviously different, but they both point to an entirely new chemical axis in the brain that could be targeted to treat depression: the glutamine/glutamate axis. Commonly abbreviated Glx, these chemicals are suppressed in people with severe depression and post-traumatic stress disorder (PTSD) and do not increase when patients take serotonin-targeting antidepressants.
The company I lead is working to develop drugs to raise Glx without the damaging side effects of ketamine or ECT. The science is promising: The FDA recently issued a biomarker letter of support, its first in psychiatry under the 21st Century Cures Act, recognizing that an increased level of Glx correlates with decreased levels of depression and that drugs targeting Glx are linked to a reduction in depression and suicidal ideation.
This is your brain on exercise: Vigorous exercise boosts critical neurotransmitters, may help restore mental health -- ScienceDaily
The researchers measured GABA and glutamate levels in two different parts of the brain immediately before and after three vigorous exercise sessions lasting between eight and 20 minutes, and made similar measurements for a control group that did not exercise. Glutamate or GABA levels increased in the participants who exercised, but not among the non-exercisers. Significant increases were found in the visual cortex, which processes visual information, and the anterior cingulate cortex, which helps regulate heart rate, some cognitive functions and emotion. While these gains trailed off over time, there was some evidence of longer-lasting effects.
"There was a correlation between the resting levels of glutamate in the brain and how much people exercised during the preceding week," Maddock said. "It's preliminary information, but it's very encouraging."
These findings point to the possibility that exercise could be used as an alternative therapy for depression. This could be especially important for patients under age 25, who sometimes have more side effects from selective serotonin reuptake inhibitors (SSRIs), anti-depressant medications that adjust neurotransmitter levels.
ADHD drugs increase brain glutamate, predict positive emotion in healthy people -- ScienceDaily
In this new study, subjects were first screened for mental and physical health and then underwent MRI spectroscopy scans designed to detect the concentration of neural compounds in specific regions of their brain. From the medical literature on psychostimulants, White and her team wanted to look in the anterior cingulate cortex, which is a "hub" brain region that connects multiple brain networks involved in emotion, decision-making and behavior.
They found that two ADHD medications, d-amphetamine and Desoxyn, significantly increased the overall amount of glutamate in the right dorsal anterior cingulate cortex, even after controlling for possible confounding factors, such as volume of gray matter in the region. The rise in brain glutamate predicted both the duration and the intensity of positive emotion, measured by participant ratings about whether they liked the drug or felt high after consuming it.
