Brain-derived Neurotrophic Factor
Brain-derived Neurotrophic Factor - Related Videos
07:53
Generating a Blood-Brain Barrier Chip Using iPSC-derived Precursor Cells
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2025
This video showcases creating a blood-brain barrier chip using iPSC-derived precursor cells. It involves seeding neural progenitor cells and brain microvascular endothelial cells in separate channels with a porous membrane. By flowing differentiation media, the endothelial cells form tight junctions resembling blood vessels, and the neural cells mature into various brain cell types, establishing a functional blood-brain barrier on the chip.
14:26
Progenitor-derived Oligodendrocyte Culture System from Human Fetal Brain
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Cited by 38 •
2012
Primary, human fetal brain-derived, multipotential progenitor cells proliferate in vitro while maintaining the capacity to differentiate into neurons and astrocytes. This work shows that neural progenitors can be induced to differentiate through stages of the oligodendrocytic lineage by conditioning with select growth factors.
05:23
Developing Human iPSC-Derived Motor Nerve Organoids Using a Microfluidic Chip
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2025
This video demonstrates the method of creating motor nerve organoids by first culturing human induced pluripotent stem cells in a special medium to form spheroids, then differentiating them into motor neurons using specific inhibitors, and finally cultivating them in a microfluidic chip to extend axons and form motor nerve organoids.
11:01
Isolation and Culture of Adult Zebrafish Brain-derived Neurospheres
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Cited by 28 •
2016
Here we provide a reproducible method to examine adult neurogenesis using a neurosphere assay derived from the whole brain or from either the telencephalic, tectal or cerebellar regions of the adult zebrafish brain. Additionally, we describe the procedure to manipulate gene expression in zebrafish neurospheres.
05:18
Derivation of Leptomeninges Explant Cultures from Postmortem Human Brain Donors
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Cited by 5 •
2017
The leptomeninges explant culture protocol from human postmortem brain is a technically robust and simple way to derive fibronectin-positive meningeal fibroblasts within 6-8 weeks and cryopreserve approximately 20-30 million cells.
FAQs
Binding of BDNF to TrkB initiates several intracellular signaling routes rather than producing a single cellular response. The PI3K/Akt, MAPK/ERK, and PLCγ pathways connect receptor activation with changes in gene expression, metabolism, and synaptic function. This network helps explain how one neurotrophin can influence both neuronal regulation and synaptic processes relevant to plasticity.
These signaling pathways are important because they translate TrkB activation into several classes of cellular change. In the supplied framework, their downstream effects include regulation of gene expression, metabolism, and synaptic function. Examining the pathways therefore helps connect molecular receptor activity with broader changes in nervous-system function and plasticity.
Variation can occur in how much BDNF is present, how effectively it engages TrkB, or how strongly downstream signaling is activated. The overview specifically links altered BDNF levels or activity with depression, neurodegenerative disease, and neurological injury. Considering both abundance and signaling activity gives researchers a more complete framework for interpreting changes in neural function.
BDNF signaling provides a molecular link between synaptic plasticity and functions such as learning and memory. Because the pathway influences synaptic function, researchers can examine how receptor activation and downstream signaling relate to these cognitive processes. This connection also makes BDNF relevant when studying changes in cognition associated with neurological disease or injury.
BDNF is of interest as a biomarker because altered levels or activity have been associated with several medical conditions. A biomarker study can therefore examine whether BDNF-related measurements correspond with depression, neurodegenerative disease, or neurological injury. Interpreting such findings alongside TrkB signaling is important because concentration alone may not represent the pathway’s functional activity.
After neurological injury, BDNF research focuses on whether its signaling can contribute to nervous-system repair, neural resilience, and recovery. The therapeutic interest arises from the pathway’s links to neuronal survival, development, and synaptic plasticity. In medicine, this work supports investigation of approaches that could promote recovery, while such therapies remain research goals rather than established clinical outcomes.