Publications by authors named "L Birnbaumer"
encodes the alpha subunit of the heterotrimeric Go protein. Despite being the most abundant G protein at synapses, the role of Go in the brain remains unclear, primarily because of the high mortality associated with developmental and epileptic encephalopathy (DEE) 17 in mutated animals. Here, we conducted proteomic analyses with a brain synaptosomal fraction to investigate the Go-interactome and then generated a non-DEE model using mice to selectively knockout (KO) the presynaptic Gαo within cerebellum.
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- Researchers used genetically engineered mice and cell lines to study how the depletion of endoplasmic reticulum (ER) calcium stores activates specific calcium entry channels (SOCE) that primarily rely on Orai1 molecules.
- They discovered that Orai1 is the dominant calcium entry pathway compared to Orai2 and Orai3, and this process does not require functional TRPC molecules, as shown by experiments using cells with inactive TRPC genes.
- The study also found that even though the TRPC genes were disrupted, both store-depletion-activated calcium entry and receptor-operated calcium entry (ROCE) still relied on Orai1, leading to the establishment of a new strain of mice called TRPC heptaKO mice, which are
Most neurons are influenced by multiple neuromodulatory inputs that converge on common effectors. Mechanisms that route these signals are key to selective neuromodulation but are poorly understood. G protein-gated inwardly rectifying K (GIRK or Kir3) channels mediate postsynaptic inhibition evoked by G protein-coupled receptors (GPCRs) that signal via inhibitory G proteins.
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- * Research in mice shows that the absence of certain TRPC channel proteins (specifically TRPC5) leads to a significant reduction in adrenaline release during insulin-induced hypoglycemia.
- * There is a newly identified signaling pathway where specific receptor activation leads to TRPC5 channel stimulation, impacting adrenaline secretion, with similar plasma metabolite changes noted in both TRPC5-deficient mice and HAAF patients.
Article Synopsis
- Research shows that TRPC3 and TRPC6 channels are key players in mechanical pain hypersensitivity, commonly experienced by patients with tissue inflammation or injury.
- When these channels are knocked out in animal models, there is a reduction in pain sensitivity by decreasing the excitability of certain pain-sensing neurons.
- Targeting TRPC3 and TRPC6 may provide a promising treatment option for managing mechanical pain with fewer side effects.