The unique complexity of Purkinje cell dendrites is intimately linked to the function of its climbing fiber input. In the perceptron analogy suggested by Brunel and Barbour in 2004, synaptic weight optimization takes place at many thousands of parallel fiber inputs to each Purkinje cell under the control of instructive climbing fiber signaling. The assumption that one Purkinje cell in the adult brain receives one climbing fiber from the inferior olive has been accepted as one of the pillars and one of the few certainties in cerebellar research. Our recent finding that Purkinje cells with a higher complexity in dendritic architecture – rare in the mouse, but almost universal in human – may receive two or more climbing fiber inputs has challenged this assumption and leads to the question what the consequences of multi-innervation are. In this seminar, I will present findings on compartmental signaling independence, and will share observations on how critical balancing the robustness of climbing fiber signaling may be for proper brain function.
Christian Hansel is a Professor of Neurobiology at the University of Chicago. He studied biology at the University of Würzburg (Germany) and zoology at the University of Zurich (Switzerland), before joining the lab of Wolf Singer at the Max-Planck-Institute for Brain Research in Frankfurt (Germany) for his Ph.D., where he did research on calcium thresholds in the control of long-term potentiation (LTP) and depression (LTD) at excitatory synapses onto L2/3 pyramidal neurons in rat visual cortex. He then was a postdoc with David Linden at Johns Hopkins University, where he investigated the developmental elimination and adult plasticity of climbing fiber synapses onto Purkinje cells. In 2000, he set up his research group at the Erasmus University Medical Center in Rotterdam (The Netherlands), where his work mostly focused on the interaction of LTD and LTP pathways at parallel fiber to Purkinje cell synapses. In 2008, he moved his research group to Chicago, where his team studies synaptic and non-synaptic plasticity in the cerebellum and neocortex, as well as cellular alterations in autism.