Disease relevance of bdnf-A

• Expression of the neurotrophin brain-derived neurotrophic factor (BDNF) and its receptor trkB in the ganglion cell layer of the Xenopus retina during retinal ganglion cell (RGC) dendritic arborization indicates that BDNF is spatially and temporally available to influence RGC morphological differentiation (; ) [1].

High impact information on bdnf-A

• Synaptic potentiation induced by brain-derived neurotrophic factor (BDNF), but not neurotrophin 3, was prevented by blockers of adenosine 3',5'-monophosphate (cAMP) signaling [2].
• Increasing BDNF levels significantly increased both axon arborization and synapse number, with BDNF increasing synapse number per axon terminal [3].
• Brief depolarization in the presence of low-level BDNF results in a marked potentiation of both evoked and spontaneous synaptic transmission, whereas exposure to either BDNF or depolarization alone is without effect [4].
• BDNF treatment rescued synapses affected by NMDA receptor blockade: BDNF maintained GFP-synaptobrevin cluster density by maintaining their addition rate and rapidly inducing their stabilization [5].
• To obtain a second measure of the role of BDNF during synapse stabilization, we injected recombinant BDNF in tadpoles with altered glutamate receptor transmission in the optic tectum [5].

Biological context of bdnf-A

• Consistent with previous reports, the predicted amino acid sequences obtained in this manner from monkey and rat were identical to other mammalian BDNF sequences [6].
• The chicken and Xenopus BDNF sequences are also highly conserved, but contain 7 and 8 amino acid substitutions, respectively, compared to mammalian BDNF [6].
• Taken together, our results suggest the presence of cross-talk between Ca2+- and cAMP-signaling pathways involved in the collapsing action of neurotrophins, in which the cAMP-pathway regulates the Ca2+-mediated signal transduction required for BDNF-induced collapse [7].
• TrkB activation by brain-derived neurotrophic factor inhibits the G protein-gated inward rectifier Kir3 by tyrosine phosphorylation of the channel [8].

Anatomical context of bdnf-A

• BDNF coexists with POMC and alphaMSH within secretory granules [9].
• BDNF-induced growth cone collapse was only observed in 6 hr cultures but not in 24 hr cultures [7].
• The BDNF-induced lamellipodia appeared within minutes, rapidly protruded to their greatest extent in about 10 min, and gradually disappeared thereafter, leaving behind newly formed thin lateral processes [10].
• Bath application of BDNF induced extensive formation of lamellipodia simultaneously at multiple sites along the neurite shaft as well as at the growth cone [10].
• Critical role of TrkB and brain-derived neurotrophic factor in the differentiation and survival of retinal pigment epithelium [11].

Associations of bdnf-A with chemical compounds

• The BDNF effect required specific tyrosine residues in the amino terminus of Kir3.1 and Kir3.4 channels [8].
• 4 channels to phenylalanine significantly blocked the BDNF-induced inhibition [8].
• The general tyrosine kinase inhibitors genistein, Gö 6976, and K252a but not the serine/threonine kinase inhibitor staurosporine blocked the BDNF-induced inhibition of the channel [8].
• Superfusion and (3)H-amino acid incorporation studies demonstrated that BDNF stimulates the release of alpha-MSH and the biosynthesis of its precursor protein, POMC [12].
• Double gold-immunolabelling revealed that BDNF coexists in these granules with mesotocin [13].

Other interactions of bdnf-A

• The SSC frequency increased markedly right after a train stimulation, which was defined as post-train potentiation (PTrP), when the cultures were plated onto fibronectin substratum and chronically treated with brain-derived neurotrophic factor (BDNF) [14].
• Here, we report that TRP-like channel activity exists in the growth cones of cultured Xenopus neurons and can be modulated by exposure to netrin-1 and brain-derived neurotrophic factor, two chemoattractants for axon guidance [15].

Analytical, diagnostic and therapeutic context of bdnf-A

• We studied the subcellular distribution of BDNF in Xenopus melanotropes using a combination of high-pressure freezing, cryosubstitution and immunoelectron microscopy [9].
• We have used the polymerase chain reaction (PCR) to amplify and clone coding sequences of the mature region of brain-derived neurotrophic factor (BDNF) from monkey, rat, chicken and Xenopus genomic DNA [6].
• Fluorescent in situ hybridization studies showed a precise co-expression of BDNF and its receptor trkB in the retinal neuroepithelium and actively differentiating RPE; in vitro studies demonstrated survival- and differentiation-promoting effects in serum-free explants and dissociated cultures [11].
• Real-time quantitative RT-PCR showed that levels of BDNF mRNA in melanotrope cells are about 25 times higher in black- than in white-adapted animals [12].
• Using Western blotting and immunocytochemistry at the light and electron microscopical level, we have detected both the BDNF precursor and the mature BDNF protein in Xenopus melanotrope cells [12].

References