Talk:Developmental Mechanism - Apoptosis
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Cite this page: Hill, M.A. (2024, May 2) Embryology Developmental Mechanism - Apoptosis. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Developmental_Mechanism_-_Apoptosis |
2011
Type I vs type II spiral ganglion neurons exhibit differential survival and neuritogenesis during cochlear development
Neural Dev. 2011 Oct 11;6:33.
Barclay M, Ryan AF, Housley GD. Source Department of Physiology, The University of Auckland, Private Bag 92019, Auckland, New Zealand. g.housley@unsw.edu.au. Abstract ABSTRACT:
BACKGROUND: The mechanisms that consolidate neural circuitry are a major focus of neuroscience. In the mammalian cochlea, the refinement of spiral ganglion neuron (SGN) innervation to the inner hair cells (by type I SGNs) and the outer hair cells (by type II SGNs) is accompanied by a 25% loss of SGNs.
RESULTS: We investigated the segregation of neuronal loss in the mouse cochlea using β-tubulin and peripherin antisera to immunolabel all SGNs and selectively type II SGNs, respectively, and discovered that it is the type II SGN population that is predominately lost within the first postnatal week. Developmental neuronal loss has been attributed to the decline in neurotrophin expression by the target hair cells during this period, so we next examined survival of SGN sub-populations using tissue culture of the mid apex-mid turn region of neonatal mouse cochleae. In organotypic culture for 48 hours from postnatal day 1, endogenous trophic support from the organ of Corti proved sufficient to maintain all type II SGNs; however, a large proportion of type I SGNs were lost. Culture of the spiral ganglion as an explant, with removal of the organ of Corti, led to loss of the majority of both SGN sub-types. Brain-derived neurotrophic factor (BDNF) added as a supplement to the media rescued a significant proportion of the SGNs, particularly the type II SGNs, which also showed increased neuritogenesis. The known decline in BDNF production by the rodent sensory epithelium after birth is therefore a likely mediator of type II neuron apoptosis.
CONCLUSION: Our study thus indicates that BDNF supply from the organ of Corti supports consolidation of type II innervation in the neonatal mouse cochlea. In contrast, type I SGNs likely rely on additional sources for trophic support.
PMID 21989106
Who lives and who dies: Role of apoptosis in quashing developmental errors
Commun Integr Biol. 2011 Jul;4(4):495-7. Epub 2011 Jul 1.
Koto A, Miura M. Source Department of Genetics; Graduate School of Pharmaceutical Sciences; The University of Tokyo. Abstract Apoptosis is essential for normal development. Large numbers of cells are eliminated by apoptosis in early neural development and during the formation of neural connections. However, our understanding of this life-or-death decision is incomplete, because it is difficult to identify dying cells by conventional strategies. Live imaging is powerful for studying apoptosis, because it can trace a death-fated cell throughout its lifetime. The Drosophila sensory organ development is a convenient system for studying neural-cell selection via lateral inhibition. We recently showed that about 20% of the differentiating neuronal cells die during sensory organ development, which results in the characteristic spatial patterning of the sensory organs. The eliminated differentiating neurons expressed neurogenic genes and high levels of activated Notch. Thus, live imaging allowed us to document the role of apoptosis in neural progenitor selection, and revealed that Notch activation is the mechanism determining which cells die during sensory organ development.
PMID 21966582
