Naturally Occurring Neuron Death

Author(s):  
Dan H. Sanes ◽  
Thomas A. Reh ◽  
William A. Harris ◽  
Matthias Landgraf
1998 ◽  
Vol 140 (4) ◽  
pp. 911-923 ◽  
Author(s):  
Shernaz X. Bamji ◽  
Marta Majdan ◽  
Christine D. Pozniak ◽  
Daniel J. Belliveau ◽  
Raquel Aloyz ◽  
...  

Abstract. To determine whether the p75 neurotrophin receptor (p75NTR) plays a role in naturally occurring neuronal death, we examined neonatal sympathetic neurons that express both the TrkA tyrosine kinase receptor and p75NTR. When sympathetic neuron survival is maintained with low quantities of NGF or KCl, the neurotrophin brain-derived neurotrophic factor (BDNF), which does not activate Trk receptors on sympathetic neurons, causes neuronal apoptosis and increased phosphorylation of c-jun. Function-blocking antibody studies indicate that this apoptosis is due to BDNF-mediated activation of p75NTR. To determine the physiological relevance of these culture findings, we examined sympathetic neurons in BDNF−/− and p75NTR−/− mice. In BDNF−/− mice, sympathetic neuron number is increased relative to BDNF+/+ littermates, and in p75NTR−/− mice, the normal period of sympathetic neuron death does not occur, with neuronal attrition occurring later in life. This deficit in apoptosis is intrinsic to sympathetic neurons, since cultured p75NTR−/− neurons die more slowly than do their wild-type counterparts. Together, these data indicate that p75NTR can signal to mediate apoptosis, and that this mechanism is essential for naturally occurring sympathetic neuron death.


1991 ◽  
Vol 304 (2) ◽  
pp. 187-197 ◽  
Author(s):  
G. S. Sohal ◽  
S. D. Stoney ◽  
L. R. Campbell ◽  
T. Arumugam ◽  
K. Kumaresan ◽  
...  

Author(s):  
Dan H. Sanes ◽  
Thomas A. Reh ◽  
William A. Harris

1995 ◽  
Vol 12 (4) ◽  
pp. 605-610 ◽  
Author(s):  
A.J. Scheetz ◽  
Robert W. Williams ◽  
Mark W. Dubin

AbstractThe influence of postnatal neuronal activity on the magnitude of retinal ganglion cell death has been studied in cats. A constant blockade of activity in one eye starting just after birth does not change the severity of naturally occurring ganglion cell death, and as in normal animals, the ganglion cell population declines from 250,000 to 160,000 over a 4- to 6-week period. However, the population of retinal ganglion cells in the active untreated eye of monocularly deprived cats is increased 12% above normal (180,000 vs. 160,000 in each of four cases). This increase of 20,000 cells is permanent, and presumably reflects the competitive advantage in their target nuclei that the still active axons have over their silenced companions from the treated eye. Surprisingly, in one animal treated successfully for long duration with TTX in both eyes, the population of ganglion cells was elevated in both eyes (200,000 and 208,000 ganglion cells). This increase matches that achieved by early unilateral enucleation (Williams et al., 1983). Our results demonstrate that the complete blockade of activity reduces the severity of naturally occurring cell death in a population of CNS sensory neurons. The effects of unilateral blockade emphasize that the activity-dependent modulation of neuron death only occurs under conditions that do not place the inactive population of neurons at a competitive disadvantage.


1980 ◽  
Vol 9 (5) ◽  
pp. 603-614 ◽  
Author(s):  
Debra L. Giordano ◽  
Marion Murray ◽  
Timothy J. Cunningham

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