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From modulator to mediator: rapid effects of BDNF on ion channels
Abstract
Neurotrophins (NTs) are {?AUTHOR} a family of structurally related, secreted proteins that regulate the survival, differentiation and maintenance of function of different populations of peripheral and central neurons.1,2 Among these, BDNF (brain‐derived neurotrophic factor) has drawn considerable interest because both its synthesis and secretion are increased by physiological levels of activity, indicating a unique role of this neurotrophin in coupling neuronal activity to structural and functional properties of neuronal circuits. In addition to its classical neurotrophic effects, which are evident within hours or days and which usually result from changes in cellular gene expression, BDNF exerts acute effects on synaptic transmission and is involved in the induction of long‐term potentiation. Many of these rapid effects of BDNF are mediated by its modulation of ion channel properties following TrkB‐mediated activation of intracellular second messenger cascades and protein phosphorylation. However, recent reports have shown that BDNF not only acts as a modulator of ion channels, but can also directly and rapidly gate a Na+ channel, thereby assigning BDNF the properties of a classical excitatory transmitter. Thus, BDNF, in addition its role as a potent neuromodulator, emerges as an excitatory transmitter‐like substance which acutely controls resting membrane potential, neuronal excitability, synaptic transmission and participates in the induction of synaptic plasticity. BioEssays 26:1185–1194, 2004. © 2004 Wiley Periodicals, Inc.
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BDNF elicits rapid effects on synaptic transmission and membrane excitability primarily via activation of these signaling pathways downstream of TrkB.
“BDNF elicits rapid effects on synaptic transmission and membrane excitability primarily via activation of these signaling pathways downstream of its TrkB receptor (Poo, 2001;Rose et al., 2004).”
From BDNF-Dependent Recycling Facilitates TrkB Translocation to Postsynaptic Density during LTP via a Rab11-Dependent Pathway (2013) · cites this paper as Rose et al., 2004
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“Both receptors can act independently but also interact with each other.((16,17)) In addition to BDNF, TrkB receptors bind NT-4/5 albeit with a slightly lower affinity.”
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Inhibition of GABAASynaptic Responses by Brain-Derived Neurotrophic Factor (BDNF) in Rat Hippocampus
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“At postnatal day 14, when GABA is inhibitory, acute BDNF application reduces the amplitude of GABAergic currents within a few minutes.((40,43,56,57)) The long-lasting inhibition of GABAergic transmission is dependent on activation of TrkB and PLC-g, and also on the elevation Review articles”
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Metadata
- Authors
- Rose, C. R., Blum, R., Kafitz, K. W., Kovalchuk, Y., & Konnerth, A.
- Venue
- BioEssays
- Publisher
- Wiley
- Published
- 2004-10-21
- Volume
- 26
- Issue
- 11
- Pages
- 1185-1194
- ISSN
- 0265-9247
- 1521-1878
- Cited by
- 106
- References
- 12
- Language
- en
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