| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Z H Wang, Y Ji, W Shan, B Zeng, N Raksadawan, G M Pastores, T Wisniewski, E H Kolodn. Therapeutic effects of astrocytes expressing both tyrosine hydroxylase and brain-derived neurotrophic factor on a rat model of Parkinson's disease. Neuroscience. vol 113. issue 3. 2002-11-13. PMID:12150782. |
bdnf protected the dopaminergic neurons from apoptosis induced by 6-hydroxydopamine, and significantly increased the long-term survival of th-positive cells in the striatum. |
2002-11-13 |
2023-08-12 |
rat |
| Masao Koda, Masazumi Murakami, Hidetoshi Ino, Katsunori Yoshinaga, Osamu Ikeda, Masayuki Hashimoto, Masashi Yamazaki, Chikao Nakayama, Hideshige Moriy. Brain-derived neurotrophic factor suppresses delayed apoptosis of oligodendrocytes after spinal cord injury in rats. Journal of neurotrauma. vol 19. issue 6. 2002-09-13. PMID:12165137. |
these findings suggest that bdnf suppresses delayed apoptosis of oligodendrocytes after spinal cord injury, for which even delayed injections are effective. |
2002-09-13 |
2023-08-12 |
rat |
| M Palmada, S Kanwal, N J Rutkoski, C Gustafson-Brown, R S Johnson, R Wisdom, B D Carter, C Gufstafson-Brow. c-jun is essential for sympathetic neuronal death induced by NGF withdrawal but not by p75 activation. The Journal of cell biology. vol 158. issue 3. 2002-09-09. PMID:12163468. |
in contrast, brain-derived neurotrophic factor (bdnf) binding to p75 resulted in an equivalent level of apoptosis in neurons expressing cre, gfp, and uninfected cells. |
2002-09-09 |
2023-08-12 |
mouse |
| A Petersén A, K E Larsen, G G Behr, N Romero, S Przedborski, P Brundin, D Sulze. Brain-derived neurotrophic factor inhibits apoptosis and dopamine-induced free radical production in striatal neurons but does not prevent cell death. Brain research bulletin. vol 56. issue 3-4. 2002-02-07. PMID:11719268. |
furthermore, bdnf inhibited intracellular oxyradical stress triggered by dopamine, and partially blocked basal and dopamine-induced apoptosis. |
2002-02-07 |
2023-08-12 |
mouse |
| B Rohrer, M M LaVail, K R Jones, L F Reichard. Neurotrophin receptor TrkB activation is not required for the postnatal survival of retinal ganglion cells in vivo. Experimental neurology. vol 172. issue 1. 2001-12-05. PMID:11681842. |
the neurotrophins bdnf and nt-4, but not ngf, prevent the apoptosis of retinal ganglion cells that is otherwise observed after target ablation or axotomy. |
2001-12-05 |
2023-08-12 |
mouse |
| I Fariñas, K R Jones, L Tessarollo, A J Vigers, E Huang, M Kirstein, D C de Caprona, V Coppola, C Backus, L F Reichardt, B Fritzsc. Spatial shaping of cochlear innervation by temporally regulated neurotrophin expression. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 21. issue 16. 2001-08-30. PMID:11487640. |
during the period preceding apoptosis, nt-3 is expressed in supporting cells, whereas bdnf is expressed mainly in hair cells, which become postmitotic in an apical to basal temporal gradient. |
2001-08-30 |
2023-08-12 |
mouse |
| C S Von Bartheld, J E Johnso. Target-derived BDNF (brain-derived neurotrophic factor) is essential for the survival of developing neurons in the isthmo-optic nucleus. The Journal of comparative neurology. vol 433. issue 4. 2001-06-28. PMID:11304717. |
immunolabel for endogenous bdnf was sparse in pyknotic ion neurons, suggesting that ion neurons with low bdnf content were eliminated by apoptosis. |
2001-06-28 |
2023-08-12 |
chicken |
| J M Olson, A Asakura, L Snider, R Hawkes, A Strand, J Stoeck, A Hallahan, J Pritchard, S J Tapscot. NeuroD2 is necessary for development and survival of central nervous system neurons. Developmental biology. vol 234. issue 1. 2001-06-28. PMID:11356028. |
decreased levels of bdnf and higher rates of apoptosis in cerebellar granule cells of neurod2(-/-) mice indicate that neurod2 is necessary for the survival of specific populations of central nervous system neurons in addition to its known effects on cell cycle regulation and neuronal differentiation. |
2001-06-28 |
2023-08-12 |
mouse |
| K M Giehl, S Röhrig, H Bonatz, M Gutjahr, B Leiner, I Bartke, Q Yan, L F Reichardt, C Backus, A A Welcher, K Dethleffsen, P Mestres, M Meye. Endogenous brain-derived neurotrophic factor and neurotrophin-3 antagonistically regulate survival of axotomized corticospinal neurons in vivo. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 21. issue 10. 2001-06-21. PMID:11331378. |
the neurotrophins nerve growth factor (ngf), brain-derived neurotrophic factor (bdnf), and neurotrophin-3 (nt-3) promote neuronal survival via tyrosine kinase (trk) receptors, whereas ngf and bdnf can also induce apoptosis in developing neurons through p75(ntr) receptors in the absence of their respective trk receptors. |
2001-06-21 |
2023-08-12 |
mouse |
| R R Krishnamoorthy, P Agarwal, G Prasanna, K Vopat, W Lambert, H J Sheedlo, I H Pang, D Shade, R J Wordinger, T Yorio, A F Clark, N Agarwa. Characterization of a transformed rat retinal ganglion cell line. Brain research. Molecular brain research. vol 86. issue 1-2. 2001-05-10. PMID:11165366. |
serum deprivation resulted in apoptosis and supplementation with both bdnf and nt-4 in the growth media, protected the rgc-5 cells from undergoing apoptosis. |
2001-05-10 |
2023-08-12 |
rat |
| E Adachi-Usam. [Optic neuritis--from diagnosis to optic nerve transplantation]. Nippon Ganka Gakkai zasshi. vol 104. issue 12. 2001-04-19. PMID:11193941. |
to prevent the apoptosis of ganglion cells, we injected various neurotrophic factors such as bdnf, gdnf, and hsp 27 into the vitreous. |
2001-04-19 |
2023-08-12 |
mouse |
| M J Donovan, M I Lin, P Wiegn, T Ringstedt, R Kraemer, R Hahn, S Wang, C F Ibañez, S Rafii, B L Hempstea. Brain derived neurotrophic factor is an endothelial cell survival factor required for intramyocardial vessel stabilization. Development (Cambridge, England). vol 127. issue 21. 2000-12-22. PMID:11023857. |
bdnf deficiency results in a reduction in endothelial cell-cell contacts and in endothelial cell apoptosis, leading to intraventricular wall hemorrhage, depressed cardiac contractility and early postnatal death. |
2000-12-22 |
2023-08-12 |
mouse |
| N Klöcker, P Kermer, J H Weishaupt, M Labes, R Ankerhold, M Bäh. Brain-derived neurotrophic factor-mediated neuroprotection of adult rat retinal ganglion cells in vivo does not exclusively depend on phosphatidyl-inositol-3'-kinase/protein kinase B signaling. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 20. issue 18. 2000-10-18. PMID:10995840. |
repeated intraocular injections of bdnf prevent the degeneration of rgcs 14 d after on lesion most likely by inhibition of apoptosis. |
2000-10-18 |
2023-08-12 |
rat |
| A Baldi, E Calia, A Ciampini, M Riccio, A Vetuschi, A M Persico, F Kelle. Deafferentation-induced apoptosis of neurons in thalamic somatosensory nuclei of the newborn rat: critical period and rescue from cell death by peripherally applied neurotrophins. The European journal of neuroscience. vol 12. issue 7. 2000-09-19. PMID:10947807. |
nerve growth factor (ngf) or brain-derived neurotrophic factor (bdnf), applied on the ion stump alone or in combination, are able to partially rescue thalamic neurons from apoptosis. |
2000-09-19 |
2023-08-12 |
rat |
| B H Han, A D'Costa, S A Back, M Parsadanian, S Patel, A R Shah, J M Gidday, A Srinivasan, M Deshmukh, D M Holtzma. BDNF blocks caspase-3 activation in neonatal hypoxia-ischemia. Neurobiology of disease. vol 7. issue 1. 2000-03-29. PMID:10671321. |
in a model of neonatal h-i injury in postnatal day 7 rats, our previous data have shown that cell death with features of apoptosis is prominent between 6 and 24 h after h-i and that neurotrophins, particularly bdnf, can markedly protect against tissue loss. |
2000-03-29 |
2023-08-12 |
rat |
| B H Han, A D'Costa, S A Back, M Parsadanian, S Patel, A R Shah, J M Gidday, A Srinivasan, M Deshmukh, D M Holtzma. BDNF blocks caspase-3 activation in neonatal hypoxia-ischemia. Neurobiology of disease. vol 7. issue 1. 2000-03-29. PMID:10671321. |
utilizing a specific molecular marker of an apoptotic pathway, these findings demonstrate that h-i injury to the developing brain is a strong apoptotic stimulus leading to caspase-3 activation, that bdnf can block this process in vivo, and that the ability of bdnf to inhibit caspase activation and subsequent apoptosis likely accounts in large part for its protection against neuronal injury in this model. |
2000-03-29 |
2023-08-12 |
rat |
| G W Glazner, M P Mattso. Differential effects of BDNF, ADNF9, and TNFalpha on levels of NMDA receptor subunits, calcium homeostasis, and neuronal vulnerability to excitotoxicity. Experimental neurology. vol 161. issue 2. 2000-03-29. PMID:10686066. |
neurons pretreated with bdnf exhibited increased levels of the nmda receptor subunits nr1 and nr2a, which was associated with increased calcium responses to nmda and vulnerability to excitotoxic necrosis and reduced vulnerability to apoptosis. |
2000-03-29 |
2023-08-12 |
Not clear |
| G W Glazner, M P Mattso. Differential effects of BDNF, ADNF9, and TNFalpha on levels of NMDA receptor subunits, calcium homeostasis, and neuronal vulnerability to excitotoxicity. Experimental neurology. vol 161. issue 2. 2000-03-29. PMID:10686066. |
our data show that, whereas bdnf increases neuronal responses to glutamate while adnf9 and tnfalpha decrease the same, all three protect against excitotoxic apoptosis. |
2000-03-29 |
2023-08-12 |
Not clear |
| S Linnarsson, C A Willson, P Ernfor. Cell death in regenerating populations of neurons in BDNF mutant mice. Brain research. Molecular brain research. vol 75. issue 1. 2000-03-07. PMID:10648888. |
we find that cells in nestin-positive regions of both the subgranular layer of the dentate gyrus and the subventricular zone of the olfactory bulb undergo apoptosis starting 2 weeks after birth in the absence of bdnf. |
2000-03-07 |
2023-08-12 |
mouse |
| T Kurokawa, N Katai, H Shibuki, S Kuroiwa, Y Kurimoto, C Nakayama, N Yoshimur. BDNF diminishes caspase-2 but not c-Jun immunoreactivity of neurons in retinal ganglion cell layer after transient ischemia. Investigative ophthalmology & visual science. vol 40. issue 12. 1999-11-08. PMID:10549664. |
the purpose of this study was to examine the association of c-jun, caspase-1, -2, and -3 immunoreactivities and neuronal apoptosis in the retinal ganglion cell layer (gcl) and to study the effects of intravitreal brain-derived neurotrophic factor (bdnf) on the expression of these gene products in a rat model of retinal ischemia-reperfusion injury. |
1999-11-08 |
2023-08-12 |
rat |