A researcher is studying how diabetes affects ganglion cells and developing a potential treatment using sigma receptor ligands. The goal is to prevent ganglion cell death and the growth of new blood vessels that obstruct vision.
Research suggests that exposure to even small amounts of alcohol or anesthetics can trigger brain cell suicide, leading to permanent cognitive impairment. The findings support the idea that fetal alcohol syndrome is a result of toxic effects on the developing human brain.
Scientists at University of Toronto have found a major mechanism causing brain cells to die after stroke, leading to the development of new treatments. They discovered that the TRPM7 channel activates a lethal chain reaction when oxygen and nutrients are deprived, resulting in massive free radical production and cell death.
After a spinal cord injury, the body's natural response can lead to larger, more debilitating lesions in the spinal cord. Researchers found that glutamate and tumor necrosis factor-alpha (TNFa) over-stimulation cause secondary damage to white matter tissue and destroy oligodendrocytes, which protect axons.
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Researchers at Virginia Tech have identified two enzymes in Methanococcus jannaschii that may predate the cell's use of ribosomes to build proteins. These discoveries provide insight into how peptides were formed before ribosomes, expanding our knowledge of gene function and the evolution of life.
Researchers have found that administering n-acetyl cysteine can reverse changes in brain chemistry associated with cocaine craving. The study suggests a novel target for cocaine's action: the cysteine-glutamate antiporter, which pumps glutamate out of neurons.
A new study reveals that tumor necrosis factor alpha (TNF-alpha) regulates the expression of neurotransmitter receptors on neurons, affecting signal transmission and potentially providing new treatment approaches for dementia, Alzheimer's disease, stroke, epilepsy, and spinal cord injury. The research suggests a vital role for glial ce...
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A study by University of Houston researchers suggests that levels of transport molecules for glutamate increase during learning, indicating an important role in the process. This molecular cleaning crew helps clear away excess neurotransmitters, allowing effective transmission and a non-toxic environment in the brain.
Scientists have created a new transgenic rat model of amyotrophic lateral sclerosis (ALS) that can quickly test novel treatments and advance understanding of the disease. The rats carry an abnormal human gene for superoxide dismutase, which reveals the critical role of astrocytes in ALS progression.
A new study has identified the key step in simple motor learning, which involves the reduced response to glutamate in Purkinje cells. By examining this process, researchers hope to create a mouse that can't reduce the number of glutamate receptors on its Purkinje cells and test if it affects learning.
UCSF researchers identified PSD-95 protein as key link between nerve cells, suggesting possible target for treating mental retardation and nerve damage. The protein stimulates maturation of synapses, enabling brain development, learning, and memory.
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Researchers have identified the protein that transports glutamate, a key player in brain function, offering a potential new target for treating diseases such as Alzheimer's and Parkinson's. The discovery could lead to therapies that either reduce or increase glutamate release, depending on the specific condition.
Scientists found that pituitary adenylyl cyclase-activating peptide (PACAP) works in concert with glutamate to adjust the body's internal clock. Bright light at night triggers the release of both molecules, which convey information about light properties to the brain.
Researchers at Max Planck Institute for Brain Research discovered a protein in photoreceptor cells that plays a crucial role in adapting to changing light intensities. The activation of this autoreceptor triggers a negative feedback loop, reducing glutamate release and preventing signal saturation.
Researchers have discovered plant glutamate receptors, which work similarly to human receptors in the brain. This finding suggests that plants possess a signaling system for neurotransmitters, enabling potential use as a model system to study neurological functions.
Researchers found that calcium influx into mitochondria triggers neuron death, while changes in cytoplasmic calcium have a more subtle effect on cell health. The study suggests designing drugs to target mitochondria could prevent or intervene in glutamate-induced neuronal damage.
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A new study suggests that blocking glutamate activity may prevent schizophrenia-like behavior in rats. Using an experimental compound, researchers found that doses of PCP no longer triggered behavioral abnormalities when glutamate levels were normalized.
Researchers discovered lithium's dual anti-manic/anti-depressive effect by finding it stabilizes glutamate levels in mice brains, bringing them within a stable zone. This results in controlling both extremes of mania and depression in bipolar disorder patients.
A new study by Johns Hopkins Medicine suggests that prolonged hypothermic circulatory arrest (HCA) can cause an overproduction of glutamate, leading to increased risk of brain damage. The study found significant increases in glutamate levels during the cooling process, recovery period, and up to eight hours post-recovery.
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Researchers identify key signaling pathway involving glutamate, nitric oxide and CREB that resets biological clocks in animals. A five-minute flash of light can permanently alter gene expression and adjust daily rhythms.
Researchers found that a drug called MK-801 can reduce brain cell death during cardiac surgery by blocking glutamate receptors. The study used dogs and showed promising results, suggesting a potential new approach to preventing brain damage during heart surgery.