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Explore advanced electrophysiological techniques in red blood cells. This webinar covers automated patch clamp for ion channel study, highlighting the roles of Piezo1, KCa3.1, and TRPV2 in RBC functions and diseases, and the concept of Pseudo Action Potentials (PAPs) for understanding voltage-activated ion channels in RBCs. Agenda: Introduction by Artem Kondratskyi (Scientific Solutions Manager, Nanion Technologies) “Electrophysiological characterization of red blood cells using the automated patch clamp” by Nicoletta Murciano (Application Scientist, Nanion Technologies) “Pseudo Action Potentials (PAPs) in red blood cells – an approach of understanding” by Lars Kaestner (Professor, Saarland University) Joint discussion Here are a few takeaways from this webinar: 𝗥𝗲𝗱 𝗕𝗹𝗼𝗼𝗱 𝗖𝗲𝗹𝗹𝘀: Though often called "membranes without much of a cell," RBCs make up about 70% of all cells in the human body, and they are more than just simple carriers. 𝗡𝗼𝗯𝗲𝗹-𝗪𝗶𝗻𝗻𝗶𝗻𝗴 𝗗𝗶𝘀𝗰𝗼𝘃𝗲𝗿𝗶𝗲𝘀: Did you know that the groundbreaking discovery of the 𝗮𝗾𝘂𝗮𝗽𝗼𝗿𝗶𝗻 channel happened in RBCs, earning Peter Agre a Nobel Prize? 𝗟𝗼𝘄 𝗖𝗵𝗮𝗻𝗻𝗲𝗹 𝗖𝗼𝘂𝗻𝘁𝘀: With only 2-3 functional Gardos channels per cell, studying these channels has always been a challenge. 𝗥𝗕𝗖𝘀 𝗮𝗻𝗱 𝗢𝘄𝗲𝗻 𝗛𝗮𝗺𝗶𝗹𝗹: RBCs were one of the first cell types tested with patch clamp. Owen Hamill recorded the first RBCs in 1981. 𝗣𝗮𝘁𝗰𝗵 𝗖𝗹𝗮𝗺𝗽𝗶𝗻𝗴 𝗖𝗵𝗮𝗹𝗹𝗲𝗻𝗴𝗲𝘀: Small, fragile, and with low channel counts, RBCs are notoriously tough to study manually. But automated patch clamp is making it easier! 𝗣𝘀𝗲𝘂𝗱𝗼 𝗔𝗰𝘁𝗶𝗼𝗻 𝗣𝗼𝘁𝗲𝗻𝘁𝗶𝗮𝗹𝘀: Lars Kaestner introduced the concept of "pseudo action potentials" in RBCs, suggesting that even non-excitable cells like RBCs can exhibit membrane potential fluctuations similar to action potentials. 𝗣𝗶𝗲𝘇𝗼𝟭: The Piezo1 channel plays a significant role in maintaining RBC volume, shape, and overall functionality. Mutations in Piezo1 have been linked to hereditary xerocytosis, a genetic condition that leads to dehydration of RBCs and results in hemolytic anemia. 𝗧𝗥𝗣𝗩𝟮 & 𝗦𝗶𝗰𝗸𝗹𝗲 𝗖𝗲𝗹𝗹: Sickle cell patients show increased TRPV2 channel activity in RBCs, leading to more calcium influx and triggering the Gardos effect – key to understanding cell dehydration.