Articles tagged with Glutamates
A team of Indiana University neuroscientists has identified GLT1, a protein clearing glutamate from the brain, as critical to cocaine craving. The researchers found ceftriaxone, an antibiotic, increases GLT1 production and decreases craving in rats withdrawing from cocaine. This combination may lead to new treatments for addiction.
A study by Johns Hopkins researchers has discovered a connection between restless legs syndrome (RLS), insomnia and brain chemistry, suggesting that high levels of glutamate may be the key to understanding the condition. The findings could lead to a new approach in treating RLS and potentially other forms of insomnia.
A recent study from Columbia University Medical Center suggests that high levels of glutamate in the brain may trigger psychosis in individuals at risk for schizophrenia. This finding could lead to the development of a diagnostic tool to identify those at risk and new treatment strategies to prevent or slow disease progression.
A study published in Neuropsychopharmacology found a correlation between increased glutamate activity and suicidal behavior. Anti-glutamate drugs are being developed as a potential tool to prevent suicide.
Researchers found that targeting glutamate receptors in the vagus nerve may control pancreatic functions, providing new hope for treating conditions like gastro-esophageal reflux disorder. The study's findings support the idea that separate nerve pathways regulate diverse organs along the upper gastrointestinal tract.
Research reveals that genes involved in glutamatergic transmission are associated with an increased risk of depression. Drugs targeting the glutamate system may help improve current antidepressant treatment outcomes.
Researchers at University of Copenhagen mapped a previously unknown biological mechanism in the brain's blood-brain barrier, revealing its vital role in maintaining glutamate balance. The discovery has enormous potential for future drug development and could lead to new treatments for neurological diseases.
Researchers at VCU Massey Cancer Center have discovered a mechanism by which glioblastoma multiforme promotes neurodegeneration, leading to neuron death. AEG-1, an oncogene overexpressed in brain tumors, inhibits expression of EEAT2, a glutamate transporter, resulting in excitoxicity and excessive glutamate levels.
Researchers found that specific receptor variants determine the development of nerve cells' dendrites, a crucial mechanism for communication. Different cell classes use these variants to grow dendrites in unique ways.
Researchers identify a promising candidate gene, SLC6A15, involved in the regulation of glutamate, an important neurotransmitter. The study shows that changes in this gene's activity can be influenced by genetic variations and even stress, providing new insights into depression.
The study reveals a unique conformation of the GluN2D subunit that mediates slow neuronal deactivation when bound to glutamate, a key neurotransmitter. This discovery can form a basis for designing new drugs targeting this receptor variant, implicated in various neurodegenerative diseases.
Researchers found alpha cells can harm beta cells through glutamate toxicity, leading to diabetes. A protective protein called GLT1 helps regulate glutamate levels and may offer a new diagnostic test or therapeutic target.
Two new studies provide definitive evidence that administering a naturally-occurring enzyme called oxolacetate can reduce glutamate levels and improve outcomes in stroke patients. High glutamate levels correlate with poor outcomes, while high oxolacetate levels are associated with better recovery.
A new study found lower glutamate levels in the hippocampus associated with increased dopamine activity, suggesting a risk marker for later psychotic disorders. The abnormal relationship between glutamatergic and dopaminergic systems may support early treatment of psychosis.
Researchers found a link between psychosis and an abnormal connection between dopamine and glutamate in the brain, suggesting new treatment approaches for schizophrenia. The study, funded by the MRC, may lead to better drugs for preventing psychotic symptoms.
A recent study published in The Journal of Neuroscience explains the unique molecular action of memantine, a FDA-approved drug for Alzheimer's disease, that underlies its rare side effects. Memantine improves symptoms by blocking abnormal glutamate activity, sparing synaptic receptors and minimizing harm.
A new biosensor can measure real-time glutamate flux of neural cells in a living organism, providing valuable data for neurological diseases and treatments. The sensor's versatility would be valuable for understanding the effects of therapies for various conditions.
Researchers at Ohio State University found that tocotrienol form of natural vitamin E can prevent nerve cells from dying after a stroke by blocking the release of fatty acids. The study suggests that this form of vitamin E has distinct functions and offers a potential therapeutic target for preventing and treating strokes.
High concentrations of glutamate activate the metabotropic glutamate receptor 1 (mGlu1 receptors), which become protective against toxic effects. This finding may lead to rational drug design for therapeutic approaches to protect against excitotoxic brain damage following injury and neurodegenerative diseases.
Researchers have identified a receptor on the tongue that is specifically activated by glutamate, a non-essential amino acid found in many foods. This discovery sheds new light on the umami taste and challenges existing perceptions of MSG's safety.
Researchers found that patients with trichotillomania reported significantly reduced hair-pulling after taking the supplement for 12 weeks. Fifty people participated in a double-blind study, with 56% reporting improved symptoms.
Researchers investigated hepatic encephalopathy (HE) and prehepatic portal hypertension in rats. The study found increased GS activity and decreased glutamate uptake in the hippocampus, leading to CNS damage. These findings may help understand HE mechanisms and develop new treatments.
Researchers have discovered a new link between soluble amyloid beta protein and synaptic injury in Alzheimer's disease. The study reveals that amyloid beta enhances long-term synaptic depression through altered glutamate uptake at hippocampal synapses.
UCSF researchers found a correlation between glutamate toxicity and neurodegeneration in MS patients, suggesting a new method for tracking disease progression. The study's findings may lead to improved monitoring of treatment and the development of new therapies.
Recent research reveals that migraine mice have an imbalance in excitation and inhibition, leading to increased neuronal activity. Glutamate release is found to be elevated, facilitating the propagation of cortical spreading depression (CSD), a phenomenon linked to migraine aura.
A recent study in mice found that high levels of EAAT2 protein decreased abdominal pain by 50-70%. The protein acts on glutamate, preventing it from interacting with receptors that send pain signals. Researchers hope EAAT2 may treat visceral pain associated with gastrointestinal disorders like IBS.
A new UCLA study found that drinking at least three cups of green or black tea a day can significantly reduce the risk of stroke. The study suggests that the antioxidant compounds in tea, such as EGCG and theanine, may be responsible for this effect.
Researchers at Rice University have identified a potential connection between glutamate and phosphoinositide 3-kinase (PI3K) in the development of neurological disorders. A mutation in a glutamate receptor gene found in both fruit flies and humans can disrupt regulatory mechanisms, leading to increased neuronal excitability.
Researchers found that deleting the gene for glutamate transporter EAAT1 leads to increased responses to NMDA receptor antagonist MK-801, resulting in schizophrenia-like features in mice. The study suggests a promising new class of glutamate-targeting antipsychotic treatments may help correct these abnormalities.
A new study may have uncovered the cause of Devic's disease by identifying glutamate as a key player in the progression of the disease. The researchers found that an autoantibody called NMO-IgG triggers a toxic build-up of glutamate, leading to damage to nerve cells and their insulating myelin coats.
Researchers discuss inhibiting glutamate receptors as a promising approach for treating chronic pain, migraine and muscle spasticity. Glutamate receptor antagonists like tezampanel have shown potential in clinical trials for treating various conditions.
Scientists at Virginia Commonwealth University found an antibiotic that can reduce neuronal cell death in the brain, which could lead to new therapies for Alzheimer's disease and other neurodegenerative disorders. The discovery was made by identifying how a compound induces neurotransmitter activity in brain cells.
A study by Michigan Medicine researchers found that pain levels in patients with fibromyalgia decreased when glutamate levels went down. This suggests that glutamate may play a role in the disease and could be used as a biomarker of disease severity, leading to potential new treatments.
Scientists have identified nine molecules that reverse the features of fragile X syndrome in fruit flies, including deficits in learning centers and behavioral deficits. The screening also uncovered other neural pathways that may be targeted for drug therapy.
Researchers found that mice genetically engineered to lack a particular protein have profound deafness and seizures, suggesting a pathway for exploring the hereditary causes of deafness and epilepsy in humans. The study also provides new insight into the role of glutamate, a chemical messenger involved in virtually every brain function.
Researchers at UT Southwestern Medical Center uncovered the mechanism underlying Fragile X syndrome, affecting communication between brain cells. The study suggests targeting the acetylcholine system might provide an alternative to drugs targeting glutamate pathways.
Researchers at Carnegie Mellon have modeled the molecular changes that occur when glutamate docks with a receptor on a neuron, enabling computer simulation of binding-site closure and opening. This breakthrough could lead to the development of drug therapies for disorders such as epilepsy and Alzheimer’s disease.
In a groundbreaking discovery, Johns Hopkins scientists found that brain cells in the white matter communicate through electrical signals similar to those used by gray matter cells. This process allows 'naked' nerve cells to signal nearby oligodendrocyte precursor cells, potentially aiding in the repair of damaged myelin coats.
The brain's information processing is more chaotic than previously thought, with neurons releasing chemical messengers along their entire length. This challenges traditional understanding of neuronal communication and may lead to new medical drug development.
The largest search for autism genes to date has implicated components of the brain's glutamate chemical messenger system and a previously overlooked site on chromosome 11. Tiny variations in genes may heighten risk for autism spectrum disorders, with evidence pointing to gene variants affecting neurotransmitter systems.
Researchers at University of Illinois Chicago discovered that receptor numbers on nerve cells are controlled by brain's level of glutamate, a previously ignored neurotransmitter. This finding has implications for understanding perception, learning, and behavior, including homosexuality.
Researchers found a significant association between the GAD1 gene and the development of alcoholism in Han Taiwanese men. The study suggests that defects in GABA synthesis may contribute to increased alcohol consumption, leading to dependence. Further exploration of GABA's role in alcoholism may lead to new treatment strategies.
Researchers have found a significant association between OCD patients and genetic variations on the SLC1A1 gene, which regulates glutamate flow in brain cells. The study suggests that this gene may be a primary candidate for OCD, potentially leading to improved understanding and treatment of the disorder.
A genetic disorder causing hypoglycemia, congenital hyperinsulinism is linked to defects in insulin secretion by pancreatic cells. Mutations in the glutamate dehydrogenase gene impair enzyme sensitivity, leading to excessive insulin release and hypoglycemia.
A mutation in the EAAT2 gene, which regulates glutamate levels in the brain, is associated with elevated plasma glutamate and increased risk of post-stroke neurological problems. Stroke patients with the mutated allele had higher plasma glutamate levels and more severe neurological outcomes than those with the normal allele.
A team of scientists found that electric fish can store memories through the activation of ion channels called TRP channels, which remain active for a long time. This discovery could help researchers better understand memory formation and neural disorders like epilepsy in humans.
A study found that receptors on brain nerve cells bind to apolipoprotein E and glutamate, affecting memory formation. Efficient APOE levels may clog these binding sites, preventing glutamate from activating processes necessary for memories.
Studies using a laboratory model of PRODH deficiency demonstrate the role of COMT in compensating for overactive dopamine signaling, which contributes to schizophrenia symptoms. The findings show that disruptions in gene interaction, particularly between PRODH and COMT, play a crucial role in the development of schizophrenia.
Researchers at OHSU found that mice consuming fewer calories experienced a boost in essential neurochemical glutamate, which reversed a Parkinson's-induced drop. The study suggests dietary restriction may be beneficial in early-stage Parkinson's disease.
Researchers found that riluzole, a glutamate modulating agent, reduced symptoms in 35% of patients with OCD. The study suggests that riluzole may represent a novel treatment intervention for certain anxiety and mood disorders.
Researchers discover KDI tri-peptide can block glutamate's damage in degenerative brain diseases, potentially leading to paralysis reversal and nerve regeneration. Human clinical trials expected to begin next year, with no toxic side effects seen so far.
Animal research suggests a potential new treatment target for epilepsy by blocking a specific brain pathway involved in seizure spread. The treatment could be more effective and have fewer side effects than current therapies.
Researchers developed a new fluorescent imaging technique using FRET (Fluorescence Resonance Energy Transfer) to track glutamate production in individual brain cells. This breakthrough technology will help better understand disease processes and construct new drugs.
Researcher Patrice G. Guyenet proposes that central chemoreceptors are located in the retrofacial region of the brainstem, loaded with glutamate, to sense pH changes in cerebrospinal fluid. In contrast, Dr. Richerson suggests that these receptors are found near midline blood vessels to 'taste' blood pH levels.
Researchers found that immature inhibitory synapses in the auditory system release glutamate, a neurotransmitter also used by excitatory synapses, to stimulate NMDA receptors during critical brain development. This discovery could provide insight into biological causes of disorders like epilepsy and depression.
Researchers discovered that prostaglandin PGD2 has protective effects in the brain, potentially outweighing its negative consequences. The study suggests that targeting this prostaglandin may lead to new therapeutic approaches for conditions involving brain damage, such as stroke and Parkinson's disease.
A large multi-center clinical trial is planned to test the safety and efficacy of antibiotics in treating ALS. Daily injections of ceftriaxone delayed nerve damage and extended survival by 10 days in mice with a Lou Gehrig's disease model.
A new study identifies a genetic link between schizophrenia and the GRM3 gene, which regulates glutamate in brain synapses. People with the 'A' variant have lower levels of glutamate and poorer cognitive function compared to those with the 'G' variant.
Research using proton magnetic resonance spectroscopy found reduced cortical GABA levels and increased glutamate in melancholic depression patients, a subset of major depressive disorder. The study adds to evidence suggesting both GABA and glutamate systems contribute to mood disorders' pathophysiology.
Researchers at the University of Pennsylvania School of Medicine found that dysbindin protein expression is reduced in over 80% of patients with schizophrenia, correlating with increased glutamate packets. This discovery provides a critical lead for understanding schizophrenia's cellular mechanisms.