scholarly journals Effect of neonatal conductive hearing loss on neuronal size in the ventral cochlear nucleus of guinea pigs

1984 ◽  
Vol 75 (S1) ◽  
pp. S69-S69
Author(s):  
Nancy A. O'Connell
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Guinea Pigs ◽  
Conductive Hearing Loss ◽  
Ventral Cochlear Nucleus ◽  
Neuronal Size ◽  
Conductive Hearing

scholarly journals Responses of Ventral Cochlear Nucleus Neurons to Contralateral Sound After Conductive Hearing Loss

2005 ◽  
Vol 94 (6) ◽  
pp. 4234-4243 ◽  
Author(s):  
Christian J. Sumner ◽  
Debara L. Tucci ◽  
Susan E. Shore
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Conductive Hearing Loss ◽  
Normal Hearing ◽  
Inhibitory Response ◽  
Broadband Noise ◽  
Central Auditory Processing ◽  
Ventral Cochlear Nucleus ◽  
Excitatory Responses ◽  
Conductive Hearing

Conductive hearing loss (CHL) is an attenuation of signals stimulating the cochlea, without damage to the auditory end organ. It can cause central auditory processing deficits that outlast the CHL itself. Measures of oxidative metabolism show a decrease in activity of nuclei receiving input originating at the affected ear but, surprisingly, an increase in the activity of second-order neurons of the opposite ear. In normal hearing animals, contralateral sound produces an inhibitory response to broadband noise in approximately one third of ventral cochlear nucleus (VCN) neurons. Excitatory responses also occur but are very rare. We looked for changes in the binaural properties of neurons in the VCN of guinea pigs at intervals immediately, 1 day, 1 wk, and 2 wk after the induction of a unilateral CHL by ossicular disruption. CHL was always induced in the ear ipsilateral to the VCN from which recordings were made. The main observations were as follows: 1) ipsilateral excitatory thresholds were raised by at least 40 dB; 2) contralateral inhibitory responses showed a small but statistically significant immediate decrease followed by an increase, returning to normal by 14 days; and 3) there was a large increase in the proportion of units with excitatory responses to contralateral BBN. The increase was immediate and lasting. The latencies of the excitatory responses were at least 6 ms, consistent with activation by a path involving several synapses and inconsistent with cross talk. The latencies and rate-level functions of contralateral excitation were similar to those seen occasionally in normal hearing animals, suggesting an upregulation of an existing pathway. In conclusion, contralateral excitatory inputs to the VCN exist, which are not normally effective, and can compensate rapidly for large changes in afferent input.

scholarly journals Glia-related mechanisms in the anteroventral cochlear nucleus of the adult rat in response to unilateral conductive hearing loss

2014 ◽  
Vol 8 ◽  
Author(s):  
Verónica Fuentes-Santamaría ◽  
Juan C. Alvarado ◽  
Diego F. López-Muñoz ◽  
Pedro Melgar-Rojas ◽  
María C. Gabaldón-Ull ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Conductive Hearing Loss ◽  
Adult Rat ◽  
Anteroventral Cochlear Nucleus ◽  
Conductive Hearing

scholarly journals Transient Conductive Hearing Loss Regulates Cross-Modal VGLUT Expression in the Cochlear Nucleus of C57BL/6 Mice

2020 ◽  
Vol 10 (5) ◽  
pp. 260 ◽  
Author(s):  
Takaomi Kurioka ◽  
Sachiyo Mogi ◽  
Taku Yamashita
Keyword(s):  
Hearing Loss ◽  
Cell Size ◽  
Neural Plasticity ◽  
Cochlear Nucleus ◽  
Conductive Hearing Loss ◽  
Auditory Brainstem ◽  
Nerve Fibers ◽  
Sound Levels ◽  
Brainstem Response ◽  
Conductive Hearing

Auditory nerve fibers synapse onto the cochlear nucleus (CN) and are labeled using the vesicular glutamate transporter-1 (VGLUT-1), whereas non-auditory inputs are labeled using the VGLUT-2. However, the underlying regulatory mechanism of VGLUT expression in the CN remains unknown. We examined whether a sound level decrease, without primary neural damage, induces cellular and VGLUT expression change in the CN, and examined the potential for neural plasticity of the CN using unilateral conductive hearing loss models. We inserted earplugs in 8-week-old mice unilaterally for 4 weeks and subsequently removed them for another 4 weeks. Although the threshold of an auditory brainstem response significantly increased across all tested frequencies following earplug insertion, it completely recovered after earplug removal. Auditory deprivation had no significant impact on spiral ganglion and ventral CN (VCN) neurons’ survival. Conversely, although the cell size and VGLUT-1 expression in the VCN significantly decreased after earplug insertion, VGLUT-2 expression in the granule cell lamina significantly increased. These cell sizes decreased and the alterations in VGLUT-1 and -2 expression almost completely recovered at 1 month after earplug removal. Our results suggested that the cell size and VGLUT expression in the CN have a neuroplasticity capacity, which is regulated by increases and decreases in sound levels. Restoration of the sound levels might partly prevent cell size decrease and maintain VGLUT expression in the CN.

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