scholarly journals Relationship between noise-induced hearing-loss, persistent tinnitus and growth-associated protein-43 expression in the rat cochlear nucleus: does synaptic plasticity in ventral cochlear nucleus suppress tinnitus?

Neuroscience ◽  
2011 ◽  
Vol 194 ◽  
pp. 309-325 ◽  
Author(s):  
K.S. Kraus ◽  
D. Ding ◽  
H. Jiang ◽  
E. Lobarinas ◽  
W. Sun ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Synaptic Plasticity ◽  
Cochlear Nucleus ◽  
Noise Induced Hearing Loss ◽  
Ventral Cochlear Nucleus

scholarly journals Acute and Long-Term Effects of Noise Exposure on the Neuronal Spontaneous Activity in Cochlear Nucleus and Inferior Colliculus Brain Slices

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Moritz Gröschel ◽  
Jana Ryll ◽  
Romy Götze ◽  
Arne Ernst ◽  
Dietmar Basta
Keyword(s):  
Hearing Loss ◽  
Spontaneous Activity ◽  
Inferior Colliculus ◽  
Cochlear Nucleus ◽  
Noise Exposure ◽  
Brain Slices ◽  
Noise Induced Hearing Loss ◽  
Long Term Effects ◽  
Noise Trauma

Noise exposure leads to an immediate hearing loss and is followed by a long-lasting permanent threshold shift, accompanied by changes of cellular properties within the central auditory pathway. Electrophysiological recordings have demonstrated an upregulation of spontaneous neuronal activity. It is still discussed if the observed effects are related to changes of peripheral input or evoked within the central auditory system. The present study should describe the intrinsic temporal patterns of single-unit activity upon noise-induced hearing loss of the dorsal and ventral cochlear nucleus (DCN and VCN) and the inferior colliculus (IC) in adult mouse brain slices. Recordings showed a slight, but significant, elevation in spontaneous firing rates in DCN and VCN immediately after noise trauma, whereas no differences were found in IC. One week postexposure, neuronal responses remained unchanged compared to controls. At 14 days after noise trauma, intrinsic long-term hyperactivity in brain slices of the DCN and the IC was detected for the first time. Therefore, increase in spontaneous activity seems to develop within the period of two weeks, but not before day 7. The results give insight into the complex temporal neurophysiological alterations after noise trauma, leading to a better understanding of central mechanisms in noise-induced hearing loss.

scholarly journals Ventral Cochlear Nucleus Responses to Contralateral Sound Are Mediated by Commissural and Olivocochlear Pathways

2009 ◽  
Vol 102 (2) ◽  
pp. 886-900 ◽  
Author(s):  
Sanford C. Bledsoe ◽  
Seth Koehler ◽  
Debara L. Tucci ◽  
Jianxun Zhou ◽  
Colleen Le Prell ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Slow Component ◽  
Cholinergic Neurons ◽  
Tone Burst ◽  
Mechanical Destruction ◽  
Commissural Axons ◽  
Commissural Neurons ◽  
Glutamatergic Neurons ◽  
Ventral Cochlear Nucleus

In the normal guinea pig, contralateral sound inhibits more than a third of ventral cochlear nucleus (VCN) neurons but excites <4% of these neurons. However, unilateral conductive hearing loss (CHL) and cochlear ablation (CA) result in a major enhancement of contralateral excitation. The response properties of the contralateral excitation produced by CHL and CA are similar, suggesting similar pathways are involved for both types of hearing loss. Here we used the neurotoxin melittin to test the hypothesis that this “compensatory” contralateral excitation is mediated either by direct glutamatergic CN-commissural projections or by cholinergic neurons of the olivocochlear bundle (OCB) that send collaterals to the VCN. Unit responses were recorded from the left VCN of anesthetized, unilaterally deafened guinea pigs (CHL via ossicular disruption, or CA via mechanical destruction). Neural responses were obtained with 16-channel electrodes to enable simultaneous data collection from a large number of single- and multiunits in response to ipsi- and contralateral tone burst and noise stimuli. Lesions of each pathway had differential effects on the contralateral excitation. We conclude that contralateral excitation has a fast and a slow component. The fast excitation is likely mediated by glutamatergic neurons located in medial regions of VCN that send their commissural axons to the other CN via the dorsal/intermediate acoustic striae. The slow component is likely mediated by the OCB collateral projections to the CN. Commissural neurons that leave the CN via the trapezoid body are an additional source of fast, contralateral excitation.

scholarly journals Changes in microRNA Expression in the Cochlear Nucleus and Inferior Colliculus after Acute Noise-Induced Hearing Loss

2020 ◽  
Vol 21 (22) ◽  
pp. 8792
Author(s):  
Sohyeon Park ◽  
Seung Hee Han ◽  
Byeong-Gon Kim ◽  
Myung-Whan Suh ◽  
Jun Ho Lee ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Inferior Colliculus ◽  
Neural Plasticity ◽  
Cochlear Nucleus ◽  
Organ Of Corti ◽  
Auditory Pathway ◽  
Noise Induced Hearing Loss ◽  
Candidate Mirnas ◽  
Central Auditory Pathway

Noise-induced hearing loss (NIHL) can lead to secondary changes that induce neural plasticity in the central auditory pathway. These changes include decreases in the number of synapses, the degeneration of auditory nerve fibers, and reorganization of the cochlear nucleus (CN) and inferior colliculus (IC) in the brain. This study investigated the role of microRNAs (miRNAs) in the neural plasticity of the central auditory pathway after acute NIHL. Male Sprague–Dawley rats were exposed to white band noise at 115 dB for 2 h, and the auditory brainstem response (ABR) and morphology of the organ of Corti were evaluated on days 1 and 3. Following noise exposure, the ABR threshold shift was significantly smaller in the day 3 group, while wave II amplitudes were significantly larger in the day 3 group compared to the day 1 group. The organ of Corti on the basal turn showed evidence of damage and the number of surviving outer hair cells was significantly lower in the basal and middle turn areas of the hearing loss groups relative to controls. Five and three candidate miRNAs for each CN and IC were selected based on microarray analysis and quantitative reverse transcription PCR (RT-qPCR). The data confirmed that even short-term acoustic stimulation can lead to changes in neuroplasticity. Further studies are needed to validate the role of these candidate miRNAs. Such miRNAs may be used in the early diagnosis and treatment of neural plasticity of the central auditory pathway after acute NIHL.

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.

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