To die or not to die, does it change the function? Behavior of transgenic mice reveals a role for developmental cell death

@article{RondiReig2002ToDO,
  title={To die or not to die, does it change the function? Behavior of transgenic mice reveals a role for developmental cell death},
  author={Laure Rondi-Reig and Jean Mariani},
  journal={Brain Research Bulletin},
  year={2002},
  volume={57},
  pages={85-91}
}
View on Elsevier
doi.org
20 Citations
Highly Influential Citations
1
Background Citations
3
Methods Citations
1
Results Citations
1

20 Citations

Citation Type

Citation Type

Role of programmed cell death in normal neuronal development and function
TLDR
Examination of organisms where death genes have been genetically eliminated reveals that programmed cell death may play an important role in sculpting gross brain structure during early development of the neural tube.
Hyperactivity and depression-like traits in Bax KO mice
Absence of Stress Response in Dorsal Raphe Nucleus in Modulator of Apoptosis 1-Deficient Mice
TLDR
Data suggest that MOAP-1 is required in the regulation of stress response in the dorsal raphe nucleus (DRN) in young wild-type control mice, and Crosstalk between BDNF and 5-HT appears to play an important role in this stress response.
Adaptive roles of programmed cell death during nervous system development.
TLDR
The programmed cell death of developing cells is considered an essential adaptive process that evolved to serve diverse roles and perturb (inhibit) PCD is reviewed to determine the possible repercussions for nervous system development and function.
Bcl-2 over-expression fails to prevent age-related loss of calretinin positive neurons in the mouse dentate gyrus
TLDR
Data suggest an age-related loss of CR positive neurons but not total neuronal loss in normal mice and this age- related neuronal change is not prevented by Bcl-2 over-expression.
Behavioral effects of Bcl-2 deficiency: implications for affective disorders.
TLDR
The relationship between Bcl-2 and behavior is explored using mice with a targeted mutation but with a different background strain than previously tested, and the current lack of effect on anxiety measures may be related to high baseline anxiety of WTanimals.
GASTRIC INHIBITORY POLYPEPTIDE IN THE BRAIN
TLDR
This investigation investigates differences in adult hippocampal neurogenesis between male and female rats of 2 different strains and demonstrates for the first time the presence of GIP in the brain and provides evidence for a regulatory function of Gip in progenitor cell proliferation.
Dexamethasone induces apoptosis in the developing rat amygdala in an age-, region-, and sex-specific manner
NMDA receptors promote survival in somatosensory relay nuclei by inhibiting Bax-dependent developmental cell death
TLDR
The results indicate that NMDA receptors play a survival role for somatosensory relay neurons during synaptogenesis by inhibiting Bax-dependent developmental cell death.
Increased anxiety-like behaviors and mitochondrial dysfunction in mice with targeted mutation of the Bcl-2 gene: Further support for the involvement of mitochondrial function in anxiety disorders
...
1
2
...

References

SHOWING 1-10 OF 33 REFERENCES
Hu‐Bcl‐2 transgenic mice with supernumerary neurons exhibit timing impairment in a complex motor task
TLDR
This work studies motor abilities in a strain of transgenic mice with neuronal overexpression of the human Bcl‐2 protein, which have supernumerary neurons due to reduced developmental cell death, and shows that these mice have a clear deficiency in fine timing of motor coordination without impairment of basic motor functions.
Physiological and induced neuronal death are not affected in NSE‐bax transgenic mice
TLDR
In the model system, Bax overexpression did not appear to influence the in vitro survival of sensory neurons isolated from dorsal root ganglia after nerve grwoth factor (NFG) deprivation or the apoptotic death of motor neurons following axotomy.
Vision in mice with neuronal redundancy due to inhibition of developmental cell death.
TLDR
The representation of the vertical meridian was displaced by about 15% in the bcl-2 mouse, however, visual acuity, contrast threshold, and response latency were normal, indicating that compensatory mechanisms can ensure normal basic properties of vision in spite of marked neuronal redundancy.
Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice
TLDR
CPP32 is shown to play a critical role during morphogenetic cell death in the mammalian brain during embryonic day 12, resulting in a variety of hyperplasias and disorganized cell deployment.
Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia
Programmed cell death: Implications for neuropsychiatric disorders
Transgenic mice with neuronal overexpression of bcl-2 gene present navigation disabilites in a water task
Fear decrease in transgenic mice over‐expressing bcl‐2 in neurons
TLDR
Hu-bcl-2 transgenic mice showed a decrease in anxiety and neophobia, indicating that, for this particular behavior, supernumerary neurons elicit the same modification as that observed after neuronal destruction.
Behavioral alterations associated with apoptosis and down-regulation of presenilin 1 in the brains of p53-deficient mice.
Presenilin 1 (PS1) expression is repressed by the p53 tumor suppressor. As shown herein, wild-type PS1 is an effective antiapoptotic molecule capable of significantly inhibiting p53-dependent and…
Increased inferior olivary neuron and cerebellar granule cell numbers in transgenic mice overexpressing the human Bcl-2 gene.
TLDR
The increased numbers of olivary neurons suggest that bcl-2 overexpression rescues these neurons from programmed cell death, and the increase in granule cell number in only one transgenic line is discussed with respect to hypotheses that Purkinje cells regulate both granules cell progenitor proliferation and the survival of differentiated granule cells.
...
1
2
3
4
...