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Review
. 2004 Sep;22(3):123-31.
doi: 10.1080/08977190410001723308.

Brain-derived neurotrophic factor

Devin K Binder  1 , Helen E Scharfman
Affiliations
Review

Brain-derived neurotrophic factor

Devin K Binder et al. Growth Factors. 2004 Sep.

Abstract

Since the purification of BDNF in 1982, a great deal of evidence has mounted for its central roles in brain development, physiology, and pathology. Aside from its importance in neural development and cell survival, BDNF appears essential to molecular mechanisms of synaptic plasticity. Basic activity-related changes in the central nervous system are thought to depend on BDNF modification of synaptic transmission, especially in the hippocampus and neocortex. Pathologic levels of BDNF-dependent synaptic plasticity may contribute to conditions such as epilepsy and chronic pain sensitization, whereas application of the trophic properties of BDNF may lead to novel therapeutic options in neurodegenerative diseases and perhaps even in neuropsychiatric disorders.

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Figures

FIGURE 1
FIGURE 1
Multiple potential effects of local BDNF release at glutamatergic synapses. LEFT: Postsynaptic mechanisms. Top: BDNF released from dense core vesicles diffuses across the synaptic cleft to activate full-length trkB receptors (shown dimerized, trkB TK+) located at synapses on postsynaptic dendritic spines. Bottom: Postsynaptic signal transduction leads to protein phosphorylation, such as the NR2B subunit of the NMDA receptor, as well as other actions, leading to enhanced synaptic transmission. Note that the site of transcription could be the nucleus, as shown, or occur locally in the dendrite. CENTER: Presynaptic mechanisms. Top: BDNF activates, in an autocrine fashion, full-length trkB receptors on the plasma membrane of the axon terminal. Bottom: Presynaptic trkB activation leads to increased neurotransmitter release by several potential mechanisms. RIGHT: Synaptic modulation by glial cells. Top: When BDNF is released into the synaptic cleft, it may bind to receptors on juxtaposed glial cells, such as truncated trkB (trkB TK − ), possibly full-length trkB (not shown) or p75 receptors. Bottom: Activation of truncated trkB has the potential to modulate glial Ca2+ signalling, and p75 activation can initiate other pathways; both could ultimately lead to changes in synaptic transmission.
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