Neurotrophin-evoked rapid excitation through TrkB receptors

Karl W. Kafitz, Christine R. Rose, Hans Thoenen and Arthur Konnerth ()
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Karl W. Kafitz: Institut für Physiologic, Technische Universität München
Christine R. Rose: Institut für Physiologic, Technische Universität München
Hans Thoenen: Max-Plack-Institut für Neurobiologie
Arthur Konnerth: Institut für Physiologic, Technische Universität München

Nature, 1999, vol. 401, issue 6756, 918-921

Abstract: Abstract Neurotrophins are a family of structurally related proteins that regulate the survival, differentiation and maintenance of function of different populations of peripheral and central neurons1,2,3. They are also essential for modulating activity-dependent neuronal plasticity4,5,6,7. Here we show that neurotrophins elicit action potentials in central neurons. Even at low concentrations, brain-derived neurotrophic factor (BDNF) excited neurons in the hippocampus, cortex and cerebellum. We found that BDNF and neurotrophin-4/5 depolarized neurons just as rapidly as the neurotransmitter glutamate, even at a more than thousand-fold lower concentration. Neurotrophin-3 produced much smaller responses, and nerve growth factor was ineffective. The neurotrophin-induced depolarization resulted from the activation of a sodium ion conductance which was reversibly blocked by K-252a, a protein kinase blocker which prefers tyrosine kinase Trk receptors8. Our results demonstrate a very rapid excitatory action of neurotrophins, placing them among the most potent endogenous neuro-excitants in the mammalian central nervous system described so far.

Date: 1999
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DOI: 10.1038/44847

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