NMDA receptors tagged posts

New finding on Elusive Brain Receptor sheds light on what may Kill Neurons after Stroke

N3A receptor site

The N3A receptor, as modeled here by the UB researchers, may be silent under normal conditions, but can be reactivated through the unique site (in red) under acidic conditions, such as after a stroke or seizure.

Strokes, seizures, traumatic brain injury and schizophrenia: these conditions can cause persistent, widespread acidity around neurons in the brain. But exactly how that acidity affects brain function isn’t well understood. University at Buffalo researchers have begun to unravel some of the puzzle. They found that an elusive brain receptor may play an important role in the death of neurons from neurological diseases.

The UB researchers study a family of brain receptors that are critical to learning and memory, called NMDA (N-methyl-D-aspartate) receptors...

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How a Waste Product of Exercise Protects Neurons from Trauma Damage

(1) Excessive glutamate activity triggers a strong influx of calcium (Ca2+) into the neuron through NMDA receptors, which leads to cell death. (2) Lactate is transported into the neuron and (3) converted to pyruvate by the enzyme lactate dehydrogenase (LDH). (4) Pyruvate is then transported into mitochondria by the mitochondrial pyruvate carrier (MPC) where it generates ATP. (5) ATP is then released through pannexins and activates the receptor P2Y, which (6) activates the PI3K pathway. (7) This triggers the opening of potassium channels (K+), which causes the neuron to hyperpolarize, decreasing the neuron's excitability, and thus protecting it from excitotoxic damage.

(1) Excessive glutamate activity triggers a strong influx of calcium (Ca2+) into the neuron through NMDA receptors, which leads to cell death. (2) Lactate is transported into the neuron and (3) converted to pyruvate by the enzyme lactate dehydrogenase (LDH). (4) Pyruvate is then transported into mitochondria by the mitochondrial pyruvate carrier (MPC) where it generates ATP. (5) ATP is then released through pannexins and activates the receptor P2Y, which (6) activates the PI3K pathway. (7) This triggers the opening of potassium channels (K+), which causes the neuron to hyperpolarize, decreasing the neuron’s excitability, and thus protecting it from excitotoxic damage.

Researchers led by EPFL have found how lactate, a waste product of glucose metabolism can protect neurons from damage follo...

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