Disease relevance of BDNF

• By contrast, the mean percentages of surviving ganglion cells measured in eyes receiving injections of 15, 30, 60, and 90 microg BDNF at the time of the nerve damage were 52%, 81%, 77%, and 70%, respectively [1].
• PURPOSE: To examine the effects of brain-derived neurotrophic factor (BDNF) in an animal model of retinal detachment [2].
• CONCLUSIONS: Axokine, but not BDNF, delays photoreceptor loss in this hereditary retinal degeneration [3].

Psychiatry related information on BDNF

• Within layer 4, the target of thalamocortical axons, BDNF mRNA is low initially and rises to high levels by the end of the critical period for ocular dominance column formation [4].

High impact information on BDNF

• Inhibition of ocular dominance column formation by infusion of NT-4/5 or BDNF [5].
• Infusion of neurotrophin-4/5 (NT-4/5) or brain-derived neurotrophic factor (BDNF) into cat primary visual cortex inhibited column formation within the immediate vicinity of the infusion site but not elsewhere in the visual cortex [5].
• In contrast, 10 d monocular TTX during the critical period does not cause a lasting decrease in BDNF mRNA expression in columns pertaining to the treated eye, consistent with the nearly complete shift in physiological response properties of cortical neurons in favor of the unmanipulated eye known to result from long-term monocular deprivation [6].
• 125I-NT-3 binding was not blocked by NGF, or serum proteins, and brain-derived neurotrophic factor (BDNF) competed for it in a distinctly biphasic manner (IC50 values of 230 pM and 37 nM) [7].
• We found elevation in a number of factors as early as 3 days following the lesion, including neurotrophins BDNF, NT3, NGF and the insulin-like growth factor IGF-1 [8].

Biological context of BDNF

• The effect of BDNF on both proliferation and apoptotic cell death was examined [2].
• High doses of BDNF induce inflammation and result in a decrease in total ganglion cell survival but appear necessary to save medium-sized neurons, which are affected most severely by nerve injury [1].
• BDNF did not reduce overall cell death in the detachments or death of photoreceptors by apoptosis [2].
• Cell size measurements suggest a complex response among the different classes of cat ganglion cells; 30 microg BDNF treatment retained the highest number of large ganglion cells, whereas 90 microg minimized the loss of medium-sized neurons and retained normal proportions of large, medium, and small ganglion cells [1].
• Recent information about effects of NGF, BDNF and NTB-4/5 on cortical morphogenesis and plasticity reveals complex interactions between the cholinergic basal forebrain afferents and this neurotrophin family [9].

Anatomical context of BDNF

• Within visual cortex, BDNF mRNA is found in neurons in deep cortical layers (5 and 6) prior to eye opening, and in both deep and superficial layers (2 and 3) shortly afterwards [4].
• The results suggest that BDNF may aid in the recovery of the retina after reattachment by maintaining the surviving photoreceptor cells, by reducing the gliotic effects in Müller cells, and perhaps by promoting outer segment regeneration [2].
• BDNF enhances retinal ganglion cell survival in cats with optic nerve damage [1].
• CONCLUSIONS: The data show that BDNF is an effective neuroprotectant in primate-sized eyes after optic nerve injury [1].
• We conclude that the application of BDNF to a site of lingual nerve repair has a negative effect on the long-term outcome [10].

Associations of BDNF with chemical compounds

• BDNF and NT-4/5 are ligands of the TrkB tyrosine kinase receptor [11].

Other interactions of BDNF

• In both structures, BDNF mRNA expression is maintained into adulthood, while NT-3 is undetectable in the adult [4].

Analytical, diagnostic and therapeutic context of BDNF

• To assess potential roles for neurotrophins in these processes, we have examined the developmental expression of BDNF and NT-3 mRNA in the cat's visual system using in situ hybridization [4].
• After BDNF treatment, by contrast, ocular dominance (OD) shifted towards the deprived eye in a zone extending 2.5-3.5 mm from the infusion cannula, and neurons lost their orientation selectivity [12].
• On the axonal regeneration by peripheral nerve transplantation, a combined injection of brain-derived neurotrophic factor, ciliary neurotrophic factor, and forskolin resulted in a 3.4-fold increase of beta cells with regenerated axons [13].

References