Chronic ultrastructural changes in acoustic trauma: Serial-section reconstruction of stereocilia and cuticular plates

1987 ◽  
Vol 26 (1) ◽  
pp. 65-88 ◽  
Author(s):  
M.Charles Liberman
2020 ◽  
Vol 2020 ◽  
pp. 1-22
Author(s):  
Guoxia Zhu ◽  
Yongxiang Wu ◽  
Yang Qiu ◽  
Keyong Tian ◽  
Wenjuan Mi ◽  
...  

Sound conditioning (SC) is defined as “toughening” to lower levels of sound over time, which reduces a subsequent noise-induced threshold shift. Although the protective effect of SC in mammals is generally understood, the exact mechanisms involved have not yet been elucidated. To confirm the protective effect of SC against noise exposure (NE) and the stress-related signaling pathway of its rescue, we observed target molecule changes caused by SC of low frequency prior to NE as well as histology analysis in vivo and verified the suggested mechanisms in SGNs in vitro. Further, we investigated the potential role of Hsp70 and Bmi1 in SC by targeting SOD1 and SOD2 which are regulated by the FoxO1 signaling pathway based on mitochondrial function and reactive oxygen species (ROS) levels. Finally, we sought to identify the possible molecular mechanisms associated with the beneficial effects of SC against noise-induced trauma. Data from the rat model were evaluated by western blot, immunofluorescence, and RT-PCR. The results revealed that SC upregulated Hsp70, Bmi1, FoxO1, SOD1, and SOD2 expression in spiral ganglion neurons (SGNs). Moreover, the auditory brainstem responses (ABRs) and electron microscopy revealed that SC could protect against acute acoustic trauma (AAT) based on a significant reduction of hearing impairment and visible reduction in outer hair cell loss as well as ultrastructural changes in OHCs and SGNs. Collectively, these results suggested that the contribution of Bmi1 toward decreased sensitivity to noise-induced trauma following SC was triggered by Hsp70 induction and associated with enhancement of the antioxidant system and decreased mitochondrial superoxide accumulation. This contribution of Bmi1 was achieved by direct targeting of SOD1 and SOD2, which was regulated by FoxO1. Therefore, the Hsp70/Bmi1-FoxO1-SOD signaling pathway might contribute to the protective effect of SC against AAT in a rat model.


1981 ◽  
Vol 47 (1) ◽  
pp. 117-125
Author(s):  
G. Jenkins ◽  
M.D. Bennett

In the hybrid Festuca scarisoa X drymeja where pairing is incomplete at pachytene, there is preferential pairing between the longer chromosomes of the complement. EM serial-section reconstruction of nuclei at zygotene and pachytene reveals that there is equally pronounced preferential pairing between larger centromeres. This evidence suggests that the longer chromosomes have large centromeres and that centromere volume is correlated with chromosome length. Confirmation of this comes from the comparison of the frequency distributions of observed centromere volumes and those predicted on the basis of chromosome length. Although there is a positive correlation between centromere volume and chromosome length, it is not possible to identify the centromeres of each individual chromosome within the complement because (a) the differences between the lengths of each chromosome are small and (b) the estimates of relative centromere volumes vary significantly between cells.


1990 ◽  
Vol 158 (2) ◽  
pp. 187-196 ◽  
Author(s):  
V. A. Moss ◽  
D. McEwan Jenkinson ◽  
H. Y. Elder

2002 ◽  
Vol 13 (8) ◽  
pp. 2810-2825 ◽  
Author(s):  
Mark S. Ladinsky ◽  
Christine C. Wu ◽  
Shane McIntosh ◽  
J. Richard McIntosh ◽  
Kathryn E. Howell

Incubating cells at 20°C blocks transport out of the Golgi complex and amplifies the exit compartments. We have used the 20°C block, followed by EM tomography and serial section reconstruction, to study the structure of Golgi exit sites in NRK cells. The dominant feature of Golgi structure in temperature-blocked cells is the presence of large bulging domains on the three trans-most cisternae. These domains extend laterally from the stack and are continuous with “cisternal” domains that maintain normal thickness and alignment with the other stacked Golgi cisternae. The bulging domains do not resemble the perpendicularly extending tubules associated with the trans-cisternae of control cells. Such tubules are completely absent in temperature-blocked cells. The three cisternae with bulging domains can be identified as trans by their association with specialized ER and the presence of clathrin-coated buds on the trans-most cisterna only. Immunogold labeling and immunoblots show a significant degradation of a medial- and a trans-Golgi marker with no evidence for their redistribution within the Golgi or to other organelles. These data suggest that exit from the Golgi occurs directly from three trans-cisternae and that specialized ER plays a significant role in trans-Golgi function.


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