Selective vulnerability of adult cochlear nucleus neurons to de-afferentation by mechanical compression

Sekiya, Takao; Canlon, Barbara; Viberg, Agneta; Matsumoto, Masahiro; Kojima, Ken; Ono, Kazuya; Yoshida, Atsuhiro; Kikkawa, Yuichiro; Nakagawa, Takayuki; Ito, Juichi

doi:10.1016/j.expneurol.2009.04.014

Cited by 20 publications

(17 citation statements)

References 62 publications

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“…In this way, our results confirm earlier results though for the rat cochlear nerve indicating severe neuronal loss after mechanical compression to the axons of the auditory neurons (Sekiya et al 2009). …”

Section: Compression (Crush) Injury Promoted Complete Paralysis Of Thsupporting

confidence: 93%

Nerve crush but not displacement-induced stretch of the intra-arachnoidal facial nerve promotes facial palsy after cerebellopontine angle surgery

et al. 2016

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Little is known about the reasons for occurrence of facial nerve palsy after removal of cerebellopontine angle tumors. Since the intra-arachnoidal portion of the facial nerve is considered to be so vulnerable that even the slightest tension or pinch may result in ruptured axons, we tested whether a graded stretch or controlled crush would affect the postoperative motor performance of the facial (vibrissal) muscle in rats. Thirty Wistar rats, divided into five groups (one with intact controls and four with facial nerve lesions), were used. Under inhalation anesthesia, the occipital squama was opened, the cerebellum gently retracted to the left, and the intra-arachnoidal segment of the right facial nerve exposed. A mechanical displacement of the brainstem with 1 or 3 mm toward the midline or an electromagnet-controlled crush of the facial nerve with a tweezers at a closure velocity of 50 and 100 mm/s was applied. On the next day, whisking motor performance was determined by video-based motion analysis. Even the larger (with 3 mm) mechanical displacement of the brainstem had no harmful effect: The amplitude of the vibrissal whisks was in the normal range of 50°-60°. On the other hand, even the light nerve crush (50 mm/s) injured the facial nerve and resulted in paralyzed vibrissal muscles (amplitude of 10°-15°). We conclude that, contrary to the generally acknowledged assumptions, it is the nerve crush but not the displacement-induced stretching of the intra-arachnoidal facial trunk that promotes facial palsy after cerebellopontine angle surgery in rats.

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Section: Compression (Crush) Injury Promoted Complete Paralysis Of Thsupporting

confidence: 93%

Nerve crush but not displacement-induced stretch of the intra-arachnoidal facial nerve promotes facial palsy after cerebellopontine angle surgery

et al. 2016

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“…To determine whether any changes occurred in the number of other types of neurons in the DCN, anti-NeuN antibody was used to label the majority of neurons in the DCN (Sekiya et al, 2009). Positive NeuN stained cells were found in all three layers of the DCN of the normal control, the noise exposure, and the noise/treatment groups.…”

Section: Noise Exposure Did Not Change the Number Of Neun Positive Cementioning

confidence: 99%

Selective degeneration of synapses in the dorsal cochlear nucleus of chinchilla following acoustic trauma and effects of antioxidant treatment

Chen

Choi

et al. 2012

Hearing Research

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“…Significantly, neuronal loss in the CN varies between its subdivisions, depending on whether the trauma was induced by noise exposure or mechanical compression of the auditory nerve. [1920] A correlation between noise exposure and cell death in the central auditory pathway has been reported by several studies. Following exposure to impulse noise, cell death mechanisms have been found in neurons of auditory cortex layers 2 to 6 from 6 h up to 7 days.…”

Section: Introductionmentioning

confidence: 96%

Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex

et al. 2017

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It has previously been shown that acoustic overstimulation induces cell death and extensive cell loss in key structures of the central auditory pathway. A correlation between noise-induced apoptosis and cell loss was hypothesized for the cochlear nucleus and colliculus inferior. To determine the role of cell death in noise-induced cell loss in thalamic and cortical structures, the present mouse study (NMRI strain) describes the time course following noise exposure of cell death mechanisms for the ventral medial geniculate body (vMGB), medial MGB (mMGB), and dorsal MGB (dMGB) and the six histological layers of the primary auditory cortex (AI 1–6). Therefore, a terminal deoxynucleotidyl transferase dioxyuridine triphosphate nick-end labeling assay (TUNEL) was performed in these structures 24 h, 7 days, and 14 days after noise exposure (3 h, 115 dB sound pressure level, 5–20 kHz), as well as in unexposed controls. In the dMGB, TUNEL was statistically significant elevated 24 h postexposure. AI-1 showed a decrease in TUNEL after 14 days. There was no statistically significant difference between groups for the other brain areas investigated. dMGB’s widespread connection within the central auditory pathway and its nontonotopical organization might explain its prominent increase in TUNEL compared to the other MGB subdivisions and the AI. It is assumed that the onset and peak of noise-induced cell death is delayed in higher areas of the central auditory pathway and takes place between 24 h and 7 days postexposure in thalamic and cortical structures.

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Selective vulnerability of adult cochlear nucleus neurons to de-afferentation by mechanical compression

Cited by 20 publications

References 62 publications

Nerve crush but not displacement-induced stretch of the intra-arachnoidal facial nerve promotes facial palsy after cerebellopontine angle surgery

Nerve crush but not displacement-induced stretch of the intra-arachnoidal facial nerve promotes facial palsy after cerebellopontine angle surgery

Selective degeneration of synapses in the dorsal cochlear nucleus of chinchilla following acoustic trauma and effects of antioxidant treatment

Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex

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