Abstract:
:Axonal lesions to the optic nerve (ON) induce c-Jun expression in retinal ganglion cells (RGCs) of the rat in vivo. Detailed investigations using retrograde tracers, and double labeling studies for c-Jun and regeneration-associated factors, such as the growth-associated protein GAP-43, have suggested that this upregulation of c-Jun is part of a cell body response in an abortive attempt of affected RGCs to survive and regenerate an axon. On the other hand, prolonged expression of c-Jun protein has in several paradigms of neurodegeneration been linked to the induction of apoptotic cell death. In the present study, we examined the time course and subcellular localization of c-Jun protein by immunocytochemistry on retinal sections after optic nerve crush and carried out double labeling for c-Jun protein and DNA strand breaks to detect apoptosis on the same sections. Several days after ON lesion, a subpopulation of RGCs was detected in which c-Jun protein was not confined to the nucleus, but also located in the cytoplasm. In addition, RGCs were seen that displayed morphological signs of apoptosis, DNA strand breaks, and c-Jun immunoreactivity at the same time. Therefore, c-Jun expression is not confined to intact or regenerating ganglion cells, but also occurs in cells that are destined to die. Our results suggest that the decision to undergo either fate depends on additional signaling events that modulate the transcriptional actions of c-Jun.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Isenmann S,Bähr Mdoi
10.1006/exnr.1997.6585subject
Has Abstractpub_date
1997-09-01 00:00:00pages
28-36issue
1eissn
0014-4886issn
1090-2430pii
S0014-4886(97)96585-7journal_volume
147pub_type
杂志文章abstract::A "neuroplastic" hypothesis proposes that changes in neuronal structural plasticity may underlie the aetiology of depression and the action of antidepressants. The medial prefrontal cortex (mPFC) is affected by this disorder and shows an intense expression of the polysialylated form of the neural cell adhesion molecul...
journal_title:Experimental neurology
pub_type: 杂志文章
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更新日期:2008-11-01 00:00:00
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journal_title:Experimental neurology
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pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
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更新日期:1985-12-01 00:00:00
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pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2018.06.009
更新日期:2018-09-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/0014-4886(90)90029-r
更新日期:1990-11-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/s0014-4886(05)80007-x
更新日期:1990-07-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.1997.6691
更新日期:1997-12-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2007.12.004
更新日期:2008-04-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章,评审
doi:10.1016/j.expneurol.2016.05.014
更新日期:2016-10-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/0014-4886(87)90233-0
更新日期:1987-06-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.1997.6497
更新日期:1997-07-01 00:00:00
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journal_title:Experimental neurology
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更新日期:2002-05-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.1999.7194
更新日期:1999-11-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2018.07.016
更新日期:2018-11-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2012.07.013
更新日期:2012-10-01 00:00:00
abstract::Decreases in energy metabolism following traumatic brain injury (TBI) are attributed to impairment of glycolytic flux and oxidative phosphorylation. Glucose utilization post-TBI is decreased while administration of alternative substrates has been shown to be neuroprotective. Changes in energy metabolism following TBI ...
journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2020.113289
更新日期:2020-07-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/S0014-4886(03)00334-0
更新日期:2003-12-01 00:00:00
abstract::Six patients with long-lasting spasticity resistant to different drug therapies including oral baclofen received a bolus injection of lumbar intrathecal baclofen. Electromyographic (EMG) reactions of leg muscles (soleus, tibialis anterior, quadriceps, and hamstrings) to standard stimuli and during attempts at voluntar...
journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/0014-4886(89)90078-2
更新日期:1989-02-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.2001.7684
更新日期:2001-07-01 00:00:00
abstract::Exogenous myelin- or axolemma-enriched fractions were assessed for the ability to inhibit biochemical and morphological expressions of reactive gliosis in rat optic nerve. Elvax pellets containing exogenous myelin, axolemma, whole-brain homogenate, liver, or red cell extracts or no homogenate were inserted into a dura...
journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/0014-4886(88)90108-2
更新日期:1988-05-01 00:00:00
abstract::Administration of endogenous corticosterone to intact animals induces calbindin-D28k protein in the hippocampal CA1-CA2 subfields. The fact that this effect on calbindin-D28k was shown to be specific for the hippocampus argues for a receptor-mediated effect on gene expression. In addition, chronic pretreatment with co...
journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.1997.6729
更新日期:1998-02-01 00:00:00
abstract::Traumatic axonal injury (TAI) evolves within minutes to hours following traumatic brain injury (TBI). Previous studies have identified axolemmal disruption and impaired axonal transport (AxT) as key mechanisms in the evolution of TAI. While initially hypothesized that axolemmal disruption culminates in impaired AxT, p...
journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2004.05.022
更新日期:2004-11-01 00:00:00