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PLEASE NOTE: If a candidate gives a layman's talk, the livestream will start fifteen minutes earlier.

Our brain works by sending tiny electrical signals between nerve cells. These signals, called action potentials, allow us to think, feel, and move. For these signals to work properly, they need two key structures in nerve cells: the axon initial segment (AIS), where the signal is first generated, and myelin, a fatty insulation that helps signals travel quickly and precisely.

In my PhD research, I investigated how flexible (or “plastic”) these structures are, and how their changes affect brain function. First, I studied the AIS in sensory brain areas. I discovered that its length is not fixed but changes depending on sensory experience. For example, when mice lost whisker input, the AIS grew longer; with enriched sensory stimulation, it became shorter — and these changes happened within just hours. This shows that the AIS acts as a fine-tuning mechanism, keeping brain activity in balance as experiences change. I also uncovered the molecular process behind this flexibility: a pathway that removes sodium channels from the AIS surface, making nerve cells less excitable.

In the second part of my thesis, I focused on myelin in long-range brain pathways. Using a model of partial myelin loss, I showed that even subtle disruptions in myelin led to signal failures and mistimed communication between brain regions. This impaired the ability of nerve cells to integrate sensory information with feedback signals.

Together, these findings show how the AIS and myelin act as “electrical gears” of the brain, keeping our neural circuits adaptable and precise.