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Robert Blum
Researcher at University of Würzburg
Publications - 88
Citations - 4846
Robert Blum is an academic researcher from University of Würzburg. The author has contributed to research in topics: Neurotrophic factors & Neurotransmission. The author has an hindex of 31, co-authored 75 publications receiving 4221 citations. Previous affiliations of Robert Blum include Ludwig Maximilian University of Munich & Saarland University.
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Directing Astroglia from the Cerebral Cortex into Subtype Specific Functional Neurons
Christophe Heinrich,Robert Blum,Susan Gascon,Giacomo Masserdotti,Pratibha Tripathi,Rodrigo Vega Sánchez,Steffen Tiedt,Timm Schroeder,Magdalena Götz,Magdalena Götz,Benedikt Berninger +10 more
TL;DR: Forced expression of single defined transcription factors can selectively and stably convert cultured astroglia into synapse-forming excitatory and inhibitory neurons.
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TRPC3 Channels Are Required for Synaptic Transmission and Motor Coordination
Jana Hartmann,Elena Dragicevic,Helmuth Adelsberger,Horst A. Henning,Martin Sumser,Joel Abramowitz,Robert Blum,Alexander Dietrich,Marc Freichel,Veit Flockerzi,Lutz Birnbaumer,Arthur Konnerth +11 more
TL;DR: Taken together, the results establish TRPC3 as a new type of postsynaptic channel that mediates mGluR-dependent synaptic transmission in cerebellar Purkinje cells and is crucial for motor coordination.
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Deletion of TrkB in adult progenitors alters newborn neuron integration into hippocampal circuits and increases anxiety-like behavior
TL;DR: Because of the specific lack of TrkB signaling in recently generated neurons a remarkably increased anxiety-like behavior was observed in mice carrying the mutation, emphasizing the contribution of adult neurogenesis in regulating mood-related behavior.
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Truncated TrkB-T1 mediates neurotrophin-evoked calcium signalling in glia cells
TL;DR: The results show that TrkB-T1 has a direct signalling role in mediating inositol-1,4,5-trisphosphate-dependent calcium release; in addition, they identify a previously unknown mechanism of neurotrophin action in the brain.
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Neurotrophin-evoked depolarization requires the sodium channel Na V 1.9
TL;DR: It is demonstrated that the tetrodotoxin-insensitive sodium channel NaV1.9 underlies the neurotrophin-evoked excitation and a mechanism of ligand-mediated sodium channel activation is revealed.