scholarly journals p75 Neurotrophin Receptor Mediates Neuronal Cell Death by Activating GIRK Channels through Phosphatidylinositol 4,5-Bisphosphate

2008 ◽  
Vol 28 (1) ◽  
pp. 315-324 ◽  
Author(s):  
E. J. Coulson ◽  
L. M. May ◽  
S. L. Osborne ◽  
K. Reid ◽  
C. K. Underwood ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Girk Channels

scholarly journals Astrocytes Protect against Isoflurane Neurotoxicity by Buffering pro-brain–derived Neurotrophic Factor

2015 ◽  
Vol 123 (4) ◽  
pp. 810-819 ◽  
Author(s):  
Creed M. Stary ◽  
Xiaoyun Sun ◽  
Rona G. Giffard
Keyword(s):  
Cell Death ◽  
Neurotrophic Factor ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Brain Derived Neurotrophic Factor ◽  
Neurotrophin Receptor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Neuronal Cultures ◽  
P75 Neurotrophin Receptor ◽  
Primary Neuronal Cultures

Abstract Background: Isoflurane induces cell death in neurons undergoing synaptogenesis via increased production of pro-brain–derived neurotrophic factor (proBDNF) and activation of postsynaptic p75 neurotrophin receptor (p75NTR). Astrocytes express p75NTR, but their role in neuronal p75NTR-mediated cell death remains unclear. The authors investigated whether astrocytes have the capacity to buffer increases in proBDNF and protect against isoflurane/p75NTR neurotoxicity. Methods: Cell death was assessed in day in vitro (DIV) 7 mouse primary neuronal cultures alone or in co-culture with age-matched or DIV 21 astrocytes with propidium iodide 24 h after 1 h exposure to 2% isoflurane or recombinant proBDNF. Astrocyte-targeted knockdown of p75NTR in co-culture was achieved with small-interfering RNA and astrocyte-specific transfection reagent and verified with immunofluorescence microscopy. proBDNF levels were assessed by enzyme-linked immunosorbent assay. Each experiment used six to eight replicate cultures/condition and was repeated at least three times. Results: Exposure to isoflurane significantly (P < 0.05) increased neuronal cell death in primary neuronal cultures (1.5 ± 0.7 fold, mean ± SD) but not in co-culture with DIV 7 (1.0 ± 0.5 fold) or DIV 21 astrocytes (1.2 ± 1.2 fold). Exogenous proBDNF dose dependently induced neuronal cell death in both primary neuronal and co-cultures, an effect enhanced by astrocyte p75NTR inhibition. Astrocyte-targeted p75NTR knockdown in co-cultures increased media proBDNF (1.2 ± 0.1 fold) and augmented isoflurane-induced neuronal cell death (3.8 ± 3.1 fold). Conclusions: The presence of astrocytes provides protection to growing neurons by buffering increased levels of proBDNF induced by isoflurane. These findings may hold clinical significance for the neonatal and injured brain where increased levels of proBDNF impair neurogenesis.

scholarly journals Chopper, a New Death Domain of the p75 Neurotrophin Receptor That Mediates Rapid Neuronal Cell Death

2000 ◽  
Vol 275 (39) ◽  
pp. 30537-30545 ◽  
Author(s):  
Elizabeth J. Coulson ◽  
Kate Reid ◽  
Manuel Baca ◽  
Kylie A. Shipham ◽  
Sarah M. Hulett ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Death Domain

Signaling of neuronal cell death by the p75NTR neurotrophin receptor

1999 ◽  
Vol 20 (1) ◽  
pp. 29-44 ◽  
Author(s):  
Elizabeth J. Coulson ◽  
Kate Reid ◽  
Perry F. Bartlett
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neurotrophin Receptor

Involvement of p75NTR in the alteration of neuronal network activity by Aβ

2019 ◽  
Author(s):  
hucheng zhao
Keyword(s):  
Neuronal Network ◽  
Hippocampal Neurons ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Network Activity ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Neuronal Viability ◽  
Neuronal Network Activity ◽  
Low Concentrations

Abstract Background：The aberrant accumulation of amyloid-beta (Aβ) in the neocortex and hippocampus is one of the initial causes of Alzheimer's disease (AD). The p75 neurotrophin receptor (p75NTR) has been proposed to mediate Aβ-induced neuronal cell death. Whether p75NTR is required for the effects of Aβ on neuronal network activity，remains unclear. Results: Our results show that low concentrations of Aβ42 did not affect neuronal viability and synapse number. However, the Aβ42 treatment decreased the neuronal network activity of cultured wild-type hippocampal neurons, including a significant decrease of Ca2+ oscillations, spontaneous postsynaptic activity and synaptic connectivity. Moreover, the Aβ42 treatment did not affect the neuronal network activity of Tg2576/p75NTR+/− and p75NTR+/− hippocampal neurons. Conclusion: These studies will shed new light on the pathogenesis of AD and aid the development of related drugs.

Role Of Neurotrophin Receptor p75NTR In Mediating Neuronal Cell Death Following Injury

2000 ◽  
Vol 27 (7) ◽  
pp. 537-541 ◽  
Author(s):  
Ej Coulson ◽  
K Reid ◽  
Ss Murray ◽  
Ss Cheema ◽  
Pf Bartlett
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neurotrophin Receptor

scholarly journals Evidence for the equilibrium between monomers and dimers of the death domain of the p75 neurotrophin receptor

2021 ◽  
Author(s):  
Zhen Li ◽  
Zhi Lin ◽  
Carlos F. Ibanez
Keyword(s):  
Room Temperature ◽  
Molecular Mechanisms ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Size Exclusion ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Death Domain ◽  
Nmr Studies ◽  
Activation Mechanisms

The p75 neurotrophin receptor (p75NTR) is an important mediator of synaptic depression and neuronal cell death, and its expression increases upon nerve injury and in neurodegenerative diseases. However, the molecular mechanisms leading to the activation of this receptor are still a matter of debate. The oligomerization properties of the death domain (DD) of p75NTR are critical for our understanding of the activation mechanisms of the receptor. In this paper, we present additional evidence supporting the existence of an equilibrium between monomeric and dimeric forms of the p75NTR DD in solution and in the absence of any other protein. Dynamic light scattering (DLS) measurements of native, untagged human p75NTR DD at room temperature yielded Rh=2.11 for this domain in 20mM phosphate buffer, corresponding to a molecular weight (MW) of approximately 19kDa, much closer to the theoretical MW of the homodimer (i.e. 21kDa) than the monomer. MWs deduced from the Rh of different control proteins used as standards were all congruent with their theoretical MWs. In addition, size-exclusion FPLC profiles of un-tagged human p75NTR DD in both HEPES and phosphate buffers revealed elution volumes corresponding to a MW of about 15kDa, which is intermediate between monomer and dimer, and indicative of dynamic monomer/dimer interconversion during the run. Together with our previous NMR studies, as well as biophysical data for other investigators, these results support the notion that the DD of p75NTR exists in equilibrium between monomers and dimers in solution, a notion that is in agreement with the oligomerization properties of all members of the DD superfamily.

Apoptosis inducing factor (AIF) is essential for neuronal cell death following transient focal cerebral ischemia

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S466-S466
Author(s):  
Carsten Culmsee ◽  
Changlian Zhu ◽  
Miriam Höhn ◽  
Stefan Landshamer ◽  
Uta Mamrak ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Transient Focal Cerebral Ischemia ◽  
Apoptosis Inducing Factor
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