Abstract
Brain-derived neurotrophic factor (BDNF) is a neurotrophin that has pleiotropic effects on neuronal morphology and synaptic plasticity that underlie hippocampal circuit development and cognition. Recent advances established that BDNF function is controlled and diversified by molecular and cellular mechanisms including trafficking and subcellular compartmentalization of different Bdnf mRNA species, pre- vs. postsynaptic release of BDNF, control of BDNF signaling by tropomyosin receptor kinase B (TrkB) receptor interactors and conversion of pro-BDNF to mature BDNF and BDNF-propeptide. Defects in these regulatory mechanisms affect dendritic spine formation and morphology of pyramidal neurons as well as synaptic integration of newborn granule cells (GCs) into preexisting circuits of mature hippocampus, compromising the cognitive function. Here, we review recent findings describing novel dynamic mechanisms that diversify and locally control the function of BDNF in hippocampal neurons.
Highlights
The correct function of the nervous system depends on the proper establishment of the synaptic contacts achieved by neurons
Brain-derived neurotrophic factor (BDNF) is highly expressed in the hippocampus where it supports a variety of functions including regulation of neuronal morphology and synaptic plasticity by binding to the high-affinity receptor tyrosine kinase, tropomyosin receptor kinase B (TrkB; Leal et al, 2015)
The most prominent type of cells that determine the tri-synaptic circuitry are the pyramidal neurons that form the pyramidal layer of CA1 and CA3 regions, and the granule cells (GCs) of the dentate gyrus
Summary
The correct function of the nervous system depends on the proper establishment of the synaptic contacts achieved by neurons. Neuronal architecture is regulated by intrinsic and extrinsic factors, among which are neurotrophins (Park and Poo, 2013). Within this family, brain-derived neurotrophic factor (BDNF) is highly expressed in the hippocampus where it supports a variety of functions including regulation of neuronal morphology and synaptic plasticity by binding to the high-affinity receptor tyrosine kinase, tropomyosin receptor kinase B (TrkB; Leal et al, 2015). Hippocampal pyramidal and dentate GCs express both TrkB and BDNF (Drake et al, 1999), and there is a large body of evidence indicating that BDNF is a relevant modulator of structural and functional synaptic plasticity in these type of excitatory neurons (Gonzalez et al, 2016; von Bohlen Und Halbach and von Bohlen Und Halbach, 2018).
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