scholarly journals Effects of cochlear synaptopathy on spontaneous and sound-evoked activity in the mouse inferior colliculus

2018 ◽  
Author(s):  
Luke A. Shaheen ◽  
M. Charles Liberman
Keyword(s):  
Inferior Colliculus ◽  
Noise Exposure ◽  
Acoustic Startle ◽  
Cell Loss ◽  
Exact Nature ◽  
Hair Cell Loss ◽  
Threshold Elevation ◽  
Compensatory Response ◽  
Auditory Responses ◽  
Evoked Activity

ABSTRACTTinnitus and hyperacusis are life-disrupting perceptual abnormalities that are often preceded by acoustic overexposure. Animal models of overexposure have suggested a link between these phenomena and neural hyperactivity, i.e. elevated spontaneous rates (SRs) and sound-evoked responses. Prior work has focused on changes in central auditory responses, with less attention paid to the exact nature of the associated peripheral damage. The demonstration that acoustic overexposure can cause cochlear nerve damage without permanent threshold elevation suggests this type of peripheral damage may be a key elicitor of tinnitus and hyperacusis in humans with normal audiograms. We addressed this idea by recording responses in the mouse inferior colliculus (IC) following a bilateral, neuropathic noise exposure. Two wks post-exposure, mean SRs were unchanged in mice recorded while awake, or under anesthesia. SRs were also unaffected by more intense, or unilateral exposures. These results suggest that neither neuropathy nor hair cell loss are sufficient to raise SRs in the IC, at least in mice. However, it’s not clear whether our mice had tinnitus. Tone-evoked rate-level functions at the CF were steeper following exposure, specifically in the region of maximal neuropathy. Furthermore, suppression driven by off-CF tones and by ipsilateral noise were also reduced. Both changes were especially pronounced in neurons of awake mice. These findings align with prior reports of elevated acoustic startle in neuropathic mice, and indicate that neuropathy may initiate a compensatory response in the central auditory system leading to the genesis of hyperacusis.

Effects of inner hair cell loss on inferior colliculus evoked potential thresholds, amplitudes and forward masking functions in chinchillas

1998 ◽  
Vol 120 (1-2) ◽  
pp. 121-132 ◽  
Author(s):  
Sandra L McFadden ◽  
Craig Kasper ◽  
Judith Ostrowski ◽  
Dalian Ding ◽  
Richard J Salvi
Keyword(s):  
Hair Cell ◽  
Inferior Colliculus ◽  
Evoked Potential ◽  
Cell Loss ◽  
Forward Masking ◽  
Hair Cell Loss ◽  
Inner Hair Cell

scholarly journals Cochlin Deficiency Protects Against Noise-Induced Hearing Loss

2021 ◽  
Vol 14 ◽  
Author(s):  
Richard Seist ◽  
Lukas D. Landegger ◽  
Nahid G. Robertson ◽  
Sasa Vasilijic ◽  
Cynthia C. Morton ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Noise Exposure ◽  
Conductive Hearing Loss ◽  
Cell Loss ◽  
Hair Cell Loss ◽  
Wild Type ◽  
Noise Trauma ◽  
Knock Out ◽  
Conductive Hearing

Cochlin is the most abundant protein in the inner ear. To study its function in response to noise trauma, we exposed adolescent wild-type (Coch+/+) and cochlin knock-out (Coch–/–) mice to noise (8–16 kHz, 103 dB SPL, 2 h) that causes a permanent threshold shift and hair cell loss. Two weeks after noise exposure, Coch–/– mice had substantially less elevation in noise-induced auditory thresholds and hair cell loss than Coch+/+ mice, consistent with cochlin deficiency providing protection from noise trauma. Comparison of pre-noise exposure thresholds of auditory brain stem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) in Coch–/– mice and Coch+/+ littermates revealed a small and significant elevation in thresholds of Coch–/– mice, overall consistent with a small conductive hearing loss in Coch–/– mice. We show quantitatively that the pro-inflammatory component of cochlin, LCCL, is upregulated after noise exposure in perilymph of wild-type mice compared to unexposed mice, as is the enzyme catalyzing LCCL release, aggrecanase1, encoded by Adamts4. We further show that upregulation of pro-inflammatory cytokines in perilymph and cochlear soft-tissue after noise exposure is lower in cochlin knock-out than wild-type mice. Taken together, our data demonstrate for the first time that cochlin deficiency results in conductive hearing loss that protects against physiologic and molecular effects of noise trauma.

scholarly journals Osmotic stabilization prevents cochlear synaptopathy after blast trauma

2018 ◽  
Vol 115 (21) ◽  
pp. E4853-E4860 ◽  
Author(s):  
Jinkyung Kim ◽  
Anping Xia ◽  
Nicolas Grillet ◽  
Brian E. Applegate ◽  
John S. Oghalai
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Hair Cells ◽  
Noise Exposure ◽  
Endolymphatic Hydrops ◽  
Surrogate Marker ◽  
Cell Loss ◽  
Hair Cell Loss ◽  
Blast Trauma

Traumatic noise causes hearing loss by damaging sensory hair cells and their auditory synapses. There are no treatments. Here, we investigated mice exposed to a blast wave approximating a roadside bomb. In vivo cochlear imaging revealed an increase in the volume of endolymph, the fluid within scala media, termed endolymphatic hydrops. Endolymphatic hydrops, hair cell loss, and cochlear synaptopathy were initiated by trauma to the mechanosensitive hair cell stereocilia and were K+-dependent. Increasing the osmolality of the adjacent perilymph treated endolymphatic hydrops and prevented synaptopathy, but did not prevent hair cell loss. Conversely, inducing endolymphatic hydrops in control mice by lowering perilymph osmolality caused cochlear synaptopathy that was glutamate-dependent, but did not cause hair cell loss. Thus, endolymphatic hydrops is a surrogate marker for synaptic bouton swelling after hair cells release excitotoxic levels of glutamate. Because osmotic stabilization prevents neural damage, it is a potential treatment to reduce hearing loss after noise exposure.

Hair Cell Loss and Synaptic Loss in Inferior Colliculus of C57BL/6 MICE

1997 ◽  
pp. 535-542
Author(s):  
Vlasta P. Spongr ◽  
Joseph P. Walton ◽  
Robert D. Frisina ◽  
Ann Marie Kazee ◽  
Dorothy G. Flood ◽  
...  
Keyword(s):  
Hair Cell ◽  
Inferior Colliculus ◽  
Cell Loss ◽  
Hair Cell Loss ◽  
Synaptic Loss

scholarly journals Susceptibility of Diabetic Mice to Noise Trauma

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Wook Kyoung Han ◽  
Eung Hyub Kim ◽  
Sun-Ae Shin ◽  
Dong-Sik Shin ◽  
Bong Jik Kim ◽  
...  
Keyword(s):  
Noise Exposure ◽  
Inflammatory Responses ◽  
Hearing Threshold ◽  
Cell Loss ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Hair Cell Loss ◽  
Wild Type ◽  
Noise Trauma ◽  
Species Production

Diabetes can lead to many end-organ complications. However, the association between diabetes and hearing loss is not well understood. Here, we investigated the effect of noise exposure on diabetic mice compared with wild-type mice. Hearing threshold shifts, histopathologic changes in the cochlea, and inflammatory responses were evaluated over time. After noise exposure, more severe hearing threshold shifts, auditory hair cell loss, and synaptopathies were notable in diabetic mice compared with wild-type mice. Moreover, increased inflammatory responses and reactive oxygen species production were observed in the ears of diabetic mice. The results demonstrated that diabetic mice are more susceptible to noise trauma.

Reduction of inhibition in the inferior colliculus after inner hair cell loss

Neuroreport ◽  
2006 ◽  
Vol 17 (14) ◽  
pp. 1493-1497 ◽  
Author(s):  
Ala Alkhatib ◽  
Ulrich W. Biebel ◽  
Jean W.T. Smolders
Keyword(s):  
Hair Cell ◽  
Inferior Colliculus ◽  
Cell Loss ◽  
Hair Cell Loss ◽  
Inner Hair Cell

Second Place — Resident Basic Science Award 1995: Mitochondrial Role in Hair Cell Survival after Injury

1995 ◽  
Vol 113 (5) ◽  
pp. 530-540 ◽  
Author(s):  
Gregory E. Hyde ◽  
Edwin W. Rubel
Keyword(s):  
Hair Cell ◽  
Cell Survival ◽  
Mitochondrial Biogenesis ◽  
Noise Exposure ◽  
Mitochondrial Protein ◽  
Cell Loss ◽  
Control Group ◽  
Cell Integrity ◽  
Hair Cell Loss ◽  
Inferior Edge

The role of mitochondrial biogenesis in hair cell survival after injury was evaluated by inhibiting mitochondrial protein synthesis with chloramphenicol and then studying the effects on hair cell survival after exposure to two different types of ototoxins, gentamicin and acoustic trauma. Seven- to 10-day-old chicks were treated with either a single injection of gentamicin (250 mg/kg) or noise (1500 Hz at 120 dB sound pressure level for 14 hours). A subset of the gentamicin- and noise-treated animals also received chloramphenicol (1200 mg/kg during a 24-hour period) through a subcutaneous osmotic pump. A control group received chloramphenicol alone (1200 mg/kg during a 24-hour period). All animals were sacrificed after 5 days, and their basilar papillae (cochleas) were prepared for scanning electron microscopy. Hair cell loss was quantified with stereologic techniques. Animals treated with chloramphenicol alone did not have any evidence of hair cell loss. Gentamicin-treated animals had characteristic hair cell loss beginning at the basal tip and tapering out along the inferior edge more distally. The addition of chloramphenicol to gentamicin treatment significantly increased hair cell loss by 30%, extending the area of hair cell loss into the superior hair cell region at the distal boundary of the lesion. Pure-tone noise exposure characteristically produced hair cell loss along the inferior edge and occasionally included hair cells along the most superior edge. Addition of chloramphenicol to noise exposure significantly increased hair cell loss by 80%, with extension of the lesion across the full width of the sensory epithelium and basally. These results demonstrate that mitochondrial biogenesis is involved in cellular responses to injury. They suggest that mitochondrial function may regulate the probability of survival after metabolic challenges to hair cell integrity.

Hearing threshold elevation precedes hair-cell loss in prestin knockout mice

2004 ◽  
Vol 126 (1) ◽  
pp. 30-37 ◽  
Author(s):  
Xudong Wu ◽  
Jiangang Gao ◽  
Yunkai Guo ◽  
Jian Zuo
Keyword(s):  
Hair Cell ◽  
Knockout Mice ◽  
Hearing Threshold ◽  
Cell Loss ◽  
Hair Cell Loss ◽  
Threshold Elevation
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