Topic: TRPM4

During metabolic stress, such as ischemic stroke, insufficient energy supply leads to ATP deprivation, resulting in ion imbalances and depolarization of cells. This results in uncontrolled glutamate release and impaired uptake by astrocytes. However, the role of elevated extracellular glutamate concentrations in exacerbating metabolic stress remains unclear. To investigate glutamate dynamics in the extracellular space during the acute phase of energy deprivation, we utilized the green-fluorescent glutamate sensor SF-iGluSnFR1. Organotypic mouse brain slice cultures were transduced with synapsi

Spinocerebellar ataxias (SCA) are a group of inherited neurodegenerative diseases. The most common SCAs are caused by an expansion of the trinucleotide CAG, which produces a polyglutamine tract in their encoded proteins, leading to their aggregation. Patients suffering from these disorders display movement impairments, and no effective treatment exists, leading to death 10-15 years after disease onset. Until now, nearly all attempts to use traditional N-methyl-d-aspartate receptor (NMDAR) antagonists to treat neurodegenerative diseases have failed. This is because NMDARs are not only promoters

We have developed a novel way to block TRPM4 channel by applying specific antibodies that bind to an extracellular region close to the channel pore. The TRPM4 antibodies include a polyclonal antibody M4P that is specific to rodent TRPM4, a monoclonal antibody M4M that is specific to human TRPM4, and most recently, a humanized antibody M4H modified from M4M.The inhibitory effect of TRPM4 antibodies is achieved via two pathways: 1) directly blocking channel activity; 2) downregulating the surface expression of TRPM4. Under disease condition such as hypoxia/ischemia, blocking TRPM4 activity by ou