Brain-derived neurotrophic factor

PDB rendering based on 1bnd.

Available structures: 1b8m, 1bnd

Identifiers

Symbol(s)

BDNF; MGC34632

External IDs

OMIM: 113505 MGI: 88145 Homologene: 7245

Gene Ontology
Molecular Function:	• protein binding • growth factor activity
Cellular Component:	• cytoplasmic membrane-bound vesicle
Biological Process:	• ureteric bud development • anti-apoptosis • negative regulation of neuroblast proliferation • axon guidance • axon target recognition • feeding behavior • neuron recognition • glutamate secretion • dendrite development • regulation of metabolic process • nerve development • mechanoreceptor differentiation • regulation of neuron apoptosis • positive regulation of neuron differentiation • regulation of retinal programmed cell death • regulation of synaptic plasticity • inner ear development

RNA expression pattern

More reference expression data

Orthologs

Human

Mouse

Entrez

627

12064

Ensembl

ENSG00000176697

ENSMUSG00000048482

Uniprot

P23560

Q541P3

Refseq

NM_001709 (mRNA)
NP_001700 (protein)

NM_001048139 (mRNA)
NP_001041604 (protein)

Location

Chr 11: 27.63 - 27.7 Mb

Chr 2: 109.48 - 109.53 Mb

Pubmed search

[2]

[3]

Brain-derived neurotrophic factor (BDNF) is a NT-3).

Although the vast majority of neurons in the mammalian brain are formed prenatally, parts of the adult brain retain the ability to grow new neurons from neural stem cells in a process known as neurogenesis. Neurotrophins are chemicals that help to stimulate and control neurogenesis, BDNF being one of the most active. Mice born without the ability to make BDNF suffer developmental defects in the brain and sensory nervous system, and usually die soon after birth, suggesting that BDNF plays an important role in normal neural development.

Despite its name, BDNF is actually found in a range of tissue and cell types, not just in the brain. It is also expressed in the retina, the CNS, motor neurons, the kidneys, and the prostate.

Effects of stress and BDNF's link in depression

Exposure to stress and the stress hormone corticosterone has been shown to decrease the antidepressants and electroconvulsive therapy) strongly increase expression of BDNF in the brain, and have been shown to protect against this atrophy.^{[citation needed]}

Mechanism of action for BDNF

LNGFR (for "low affinity nerve growth factor receptor", also known as p75).

TrkA and TrkB as well, but with less affinity.

The other LNGFR, plays a somewhat less clear role. Some researchers have shown the LNGFR binds and serves as a "sink" for neurotrophins. Cells which express both the LNGFR and the Trk receptors might therefore have a greater activity - since they have a higher "microconcentration" of the neurotrophin. It has also been shown, however, that the LNGFR may signal a cell to die via apoptosis - so therefore cells expressing the LNGFR in the absence of Trk receptors may die rather than live in the presence of a neurotrophin.

Other diseases associated with low BDNF levels

Various studies have shown possible links between low levels of BDNF and conditions such as depression, schizophrenia, Obsessive-compulsive disorder, Alzheimer's disease, Huntington's disease, Rett syndrome, and dementia, though it is still not known whether these levels represent a cause or a symptom.^{[citation needed]}

High BDNF levels

High levels of BDNF and Substance P have been found associated with increased itching in eczema^[1].

Epilepsy

Epilepsy has also been linked with polymorphisms in BDNF. Given BDNF's vital role in the development of the landscape of the brain, there is quite a lot of room for influence on the development of neuropathologies from BDNF.

Levels of both BDNF mRNA and BDNF protein are known to be up-regulated in epilepsy (Gall C, et.al. 1991). BDNF modulates excitatory and inhibitory synaptic transmission by inhibiting GABAA-receptor mediated post-synaptic currents. This provides a potential reason for the observed up-regulation.

References

^ 'Blood chemicals link' to eczema [1]

Arévalo JC, Waite J, Rajagopal R, et al (2006). "Cell survival through Trk neurotrophin receptors is differentially regulated by ubiquitination". Neuron 50 (4): 549-59. doi:10.1016/j.neuron.2006.03.044. PMID 16701206.
Yamada K, Nabeshima T (2004). "Brain-derived neurotrophic factor/TrkB signaling in memory processes.". J. Pharmacol. Sci. 91 (4): 267-70. PMID 12719654.
Pang PT, Lu B (2005). "Regulation of late-phase LTP and long-term memory in normal and aging hippocampus: role of secreted proteins tPA and BDNF.". Ageing Res. Rev. 3 (4): 407-30. doi:10.1016/j.arr.2004.07.002. PMID 15541709.
Hashimoto K, Koizumi H, Nakazato M, et al. (2005). "Role of brain-derived neurotrophic factor in eating disorders: recent findings and its pathophysiological implications.". Prog. Neuropsychopharmacol. Biol. Psychiatry 29 (4): 499-504. doi:10.1016/j.pnpbp.2005.01.007. PMID 15866349.
Tsai SJ (2007). "Increased central brain-derived neurotrophic factor activity could be a risk factor for substance abuse: Implications for treatment.". Med. Hypotheses 68 (2): 410-4. doi:10.1016/j.mehy.2006.05.035. PMID 16824691.
Bath KG, Lee FS (2006). "Variant BDNF (Val66Met) impact on brain structure and function.". Cognitive, affective & behavioral neuroscience 6 (1): 79-85. PMID 16869232.
Nair A, Vaidya VA (2006). "Cyclic AMP response element binding protein and brain-derived neurotrophic factor: molecules that modulate our mood?". J. Biosci. 31 (3): 423-34. PMID 17006024.

v • d • e NT-3

v • d • e NT-3 - NT-4 - PACAP

Categories: Peptide hormones

This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Brain-derived_neurotrophic_factor". A list of authors is available in Wikipedia.