scholarly journals NADPH Oxidase 2-Mediated Insult in the Auditory Cortex of Zucker Diabetic Fatty Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Zheng-De Du ◽  
Wei Wei ◽  
Shukui Yu ◽  
Qing-Ling Song ◽  
Ke Liu ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Nadph Oxidase ◽  
Auditory Cortex ◽  
Auditory System ◽  
Auditory Brainstem ◽  
Secondary Symptom ◽  
Zucker Diabetic Fatty Rats ◽  
Brainstem Response ◽  
Zdf Rats ◽  
Nadph Oxidase 2

Clinical data has confirmed that auditory impairment may be a secondary symptom of type 2 diabetes mellitus (T2DM). However, mechanisms underlying pathologic changes that occur in the auditory system, especially in the central auditory system (CAS), remain poorly understood. In this study, Zucker diabetic fatty (ZDF) rats were used as a T2DM rat model to observe ultrastructural alterations in the auditory cortex and investigate possible mechanisms underlying CAS damage in T2DM. The auditory brainstem response (ABR) of ZDF rats was found to be markedly elevated in low (8 kHz) and high (32 kHz) frequencies. Protein expression of NADPH oxidase 2 (NOX2) and its matching subunits P22phox, P47phox, and P67phox was increased in the auditory cortex of ZDF rats. Expression of 8-hydroxy-2-deoxyguanosine (8-OHdG), a marker of DNA oxidative damage, was also increased in the neuronal mitochondria of the auditory cortex of ZDF rats. Additionally, decreases in the mitochondrial total antioxidant capabilities (T-AOC), adenosine triphosphate (ATP) production, and mitochondrial membrane potential (MMP) were detected in the auditory cortex of ZDF rats, suggesting mitochondrial dysfunction. Transmission electron microscopy results indicated that ultrastructural damage had occurred to neurovascular units and mitochondria in the auditory cortex of ZDF rats. Furthermore, cytochrome c (Cyt c) translocation from mitochondria to cytoplasm and caspase 3-dependent apoptosis were also detected in the auditory cortex of ZDF rats. Consequently, the study demonstrated that T2DM may cause morphological damage to the CAS and that NOX2-associated mitochondrial oxidative damage and apoptosis may be partly responsible for this insult.

scholarly journals The human auditory brainstem response to running speech reveals a subcortical mechanism for selective attention

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Antonio Elia Forte ◽  
Octave Etard ◽  
Tobias Reichenbach
Keyword(s):  
Mathematical Method ◽  
Selective Attention ◽  
Auditory Cortex ◽  
Auditory Brainstem Response ◽  
Background Noise ◽  
Ecological Validity ◽  
Acoustic Stimulus ◽  
Auditory Brainstem ◽  
Brainstem Response ◽  
Target Speaker

Humans excel at selectively listening to a target speaker in background noise such as competing voices. While the encoding of speech in the auditory cortex is modulated by selective attention, it remains debated whether such modulation occurs already in subcortical auditory structures. Investigating the contribution of the human brainstem to attention has, in particular, been hindered by the tiny amplitude of the brainstem response. Its measurement normally requires a large number of repetitions of the same short sound stimuli, which may lead to a loss of attention and to neural adaptation. Here we develop a mathematical method to measure the auditory brainstem response to running speech, an acoustic stimulus that does not repeat and that has a high ecological validity. We employ this method to assess the brainstem's activity when a subject listens to one of two competing speakers, and show that the brainstem response is consistently modulated by attention.

scholarly journals Evoked Potentials Reveal Noise Exposure–Related Central Auditory Changes Despite Normal Audiograms

2020 ◽  
Vol 29 (2) ◽  
pp. 152-164 ◽  
Author(s):  
Naomi F. Bramhall ◽  
Christopher E. Niemczak ◽  
Sean D. Kampel ◽  
Curtis J. Billings ◽  
Garnett P. McMillan
Keyword(s):  
Auditory System ◽  
Noise Exposure ◽  
Otoacoustic Emission ◽  
Auditory Brainstem ◽  
Auditory Nerve Fiber ◽  
Central Auditory System ◽  
Distortion Product Otoacoustic Emission ◽  
Distortion Product ◽  
Brainstem Response ◽  
Latency Response

Purpose Complaints of auditory perceptual deficits, such as tinnitus and difficulty understanding speech in background noise, among individuals with clinically normal audiograms present a perplexing problem for audiologists. One potential explanation for these “hidden” auditory deficits is loss of the synaptic connections between the inner hair cells and their afferent auditory nerve fiber targets, a condition that has been termed cochlear synaptopathy . In animal models, cochlear synaptopathy can occur due to aging or exposure to noise or ototoxic drugs and is associated with reduced auditory brainstem response (ABR) wave I amplitudes. Decreased ABR wave I amplitudes have been demonstrated among young military Veterans and non-Veterans with a history of firearm use, suggesting that humans may also experience noise-induced synaptopathy. However, the downstream consequences of synaptopathy are unclear. Method To investigate how noise-induced reductions in wave I amplitude impact the central auditory system, the ABR, the middle latency response (MLR), and the late latency response (LLR) were measured in 65 young Veterans and non-Veterans with normal audiograms. Results In response to a click stimulus, the MLR was weaker for Veterans compared to non-Veterans, but the LLR was not reduced. In addition, low ABR wave I amplitudes were associated with a reduced MLR, but with an increased LLR. Notably, Veterans reporting tinnitus showed the largest mean LLRs. Conclusions These findings indicate that decreased peripheral auditory input leads to compensatory gain in the central auditory system, even among individuals with normal audiograms, and may impact auditory perception. This pattern of reduced MLR, but not LLR, was observed among Veterans even after statistical adjustment for sex and distortion product otoacoustic emission differences, suggesting that synaptic loss plays a role in the observed central gain. Supplemental Material https://doi.org/10.23641/asha.11977854

Neural Basis of Music Perception: Melody, Harmony, and Timbre

2019 ◽  
pp. 186-211
Author(s):  
Stefan Koelsch
Keyword(s):  
Auditory Cortex ◽  
Auditory System ◽  
Music Perception ◽  
Neural Correlates ◽  
Auditory Brainstem ◽  
Implicit Knowledge ◽  
Musical Structure ◽  
Acoustic Features ◽  
Neural Basis ◽  
Auditory Sensory Memory

During listening, acoustic features of sounds are extracted in the auditory system (in the auditory brainstem, thalamus, and auditory cortex). To establish auditory percepts of melodies and rhythms (i.e., to establish auditory “Gestalten” and auditory objects), sound information is buffered and processed in the auditory sensory memory. Musical structure is then processed based on acoustical similarities and rhythmical organization. In addition, musical structure is processed according to (implicit) knowledge about musical regularities underlying scales, melodic and harmonic progressions, and so on. These structures are based on both local and (hierarchically organized) nonlocal dependencies. This chapter reviews neural correlates of these processes, with regard to both brain-electric responses to sounds, and the neuroanatomical architecture of music perception.

scholarly journals 1α,25-Dihydroxyvitamin D3 prevents renal oxidative damage via the PARP1/SIRT1/NOX4 pathway in Zucker diabetic fatty rats

2020 ◽  
Vol 318 (3) ◽  
pp. E343-E356
Author(s):  
Dongxia Wang ◽  
Yanyan Li ◽  
Ning Wang ◽  
Gang Luo ◽  
Jun Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Oxidative Damage ◽  
Sirtuin 1 ◽  
Diabetic Rat ◽  
Membrane Thickness ◽  
Basement Membrane Thickness ◽  
Zucker Diabetic Fatty Rats ◽  
Zdf Rats ◽  
Rat Kidneys

Diabetic nephropathy (DN) is one of the most important renal complications associated with diabetes, and the mechanisms are yet to be fully understood. To date, few studies have shown the antioxidant effects of 1α,25-dihydroxyvitamin-D3 [1,25(OH)2D3] on hyperglycemia-induced renal injury. The aim of the present study was to explore the potential mechanism by which 1,25(OH)2D3 reduced oxidative stress in diabetic rat kidneys. In this study, we established a vitamin D-deficient spontaneous diabetes model: 5–6 wk of age Zucker diabetic fatty (ZDF) rats were treated with or without 1,25(OH)2D3 for 7 wk, age-matched Zucker lean rats served as control. Results showed that ZDF rats treated with 1,25(OH)2D3 had decreased body mass, food intake, water intake, and urine volume. 1,25(OH)2D3 ameliorated urine glucose, blood glucose and abnormal glucose tolerance. Additionally, 1,25(OH)2D3 significantly lowered microalbuminuria, decreased the glomerular basement membrane thickness, and in some degree inhibited glomerular hypertrophy, mesangial expansion, and tubular dilatation. Furthermore, 1,25(OH)2D3 attenuated renal oxidative damage, as reflected by the levels of malondialdehyde, reduced glutathione, 4-hydroxynonenal, 8-hydroxy-2'-deoxyguanosine, and reactive oxygen species production, and notably inhibited poly(ADP-ribose) polymerase-1 (PARP1), activated sirtuin 1 (SIRT1), and decreased the expression of NADPH oxidase 4 (NOX4). Of interest, the abovementioned proteins could be involved in the antioxidant mechanism of 1,25(OH)2D3 in diabetic rat kidneys. Our study showed that oxidative stress might be a major contributor to DN pathogenesis and uncovered the antioxidant role of 1,25(OH)2D3 in diabetic nephropathy that was associated with the PARP1/SIRT1/ NOX4 pathway.

Presbyacusis and the Auditory Brainstem Response

2002 ◽  
Vol 45 (6) ◽  
pp. 1249-1261 ◽  
Author(s):  
Flint A. Boettcher
Keyword(s):  
Hearing Loss ◽  
Auditory System ◽  
Auditory Brainstem Response ◽  
Animal Studies ◽  
Auditory Brainstem ◽  
Clinical Tool ◽  
Age Related ◽  
Brainstem Response ◽  
Auditory Functions ◽  
Age Related Changes

Age-related hearing loss (ARHL or presbyacusis) is an increasingly common form of sensorineural hearing loss (SNHL) as a result of changing demographics, and the auditory brainstem response (ABR) is a common experimental and clinical tool in audiology and neurology. Some of the changes that occur in the aging auditory system may significantly influence the interpretation of the ABR in comparison to the ABRs of younger adults. The approach of this review will be to integrate physiological and histopathological data from human and animal studies to provide a better understanding of the array of age-related changes in the ABR and to determine how age-related changes in the auditory system may influence how the ABR should be interpreted in presbyacusis. Data will be described in terms of thresholds, latencies, and amplitudes, as well as more complex auditory functions such as masking and temporal processing. Included in the review of data will be an attempt to differentiate between age-related effects that may strictly be due to threshold elevation from those that may be due to the aging process.

The miR-34a/Bcl-2 Pathway Contributes to Auditory Cortex Neuron Apoptosis in Age-Related Hearing Loss

2017 ◽  
Vol 22 (2) ◽  
pp. 96-103 ◽  
Author(s):  
Qiuhong Huang ◽  
Yongkang Ou ◽  
Hao Xiong ◽  
Haidi Yang ◽  
Zhigang Zhang ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Molecular Mechanisms ◽  
Primary Auditory Cortex ◽  
Auditory Brainstem ◽  
Hearing Ability ◽  
Age Related ◽  
Brainstem Response ◽  
The Central Nervous System ◽  
Age Related Hearing Loss

Hypothesis: The miR-34a/Bcl-2 signaling pathway may play a role in the mechanisms related to age-related hearing loss (AHL) in the auditory cortex. Background: The auditory cortex plays a key role in the recognition and processing of complex sound. It is difficult to explain why patients with AHL have poor speech recognition, so increasing numbers of studies have focused on its central change. Although micro (mi)RNAs in the central nervous system have recently been increasingly reported to be associated with age-related diseases, the molecular mechanisms of AHL in the auditory cortex are not fully understood. Methods: The auditory brainstem response was used to assess the hearing ability of C57BL/6 mice, and q-PCR, immunohistochemistry, and Western blotting were used to detect the expression levels of miR-34a and Bcl-2 in the mouse auditory cortex. TUNEL and DNA fragmentation were adopted to detect the apoptosis of neurons in the auditory cortex. To verify the relationship of miR-34a and Bcl-2, we transfected an miR-34a mimic or miR-34a inhibitor into primary auditory cortex neurons. Results: In this study, miR-34a/Bcl-2 signaling was examined in auditory cortex neurons during aging. miR-34a and apoptosis increased in the auditory cortex neurons of C57BL/6 mice with aging, whereas an age-related decrease in Bcl-2 was determined. In the primary neurons of the auditory cortex, miR-34a overexpression inhibited Bcl-2, leading to an increase in apoptosis. Moreover, miR-34a knockdown increased Bcl-2 expression and diminished apoptosis. Conclusion: Our results support a link between age-related apoptosis in auditory cortex neurons and miR-34a/Bcl-2 signaling, which may serve as a potential mechanism of the expression of AHL in the auditory cortex.

scholarly journals Development of Brainstem-Evoked Responses in Congenital Auditory Deprivation

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
J. Tillein ◽  
S. Heid ◽  
E. Lang ◽  
R. Hartmann ◽  
A. Kral
Keyword(s):  
Auditory System ◽  
Developmental Stages ◽  
Auditory Brainstem ◽  
Acute Experiment ◽  
Auditory Brainstem Responses ◽  
Evoked Responses ◽  
Auditory Deprivation ◽  
Stimulus Artifact ◽  
Brainstem Response ◽  
Monopolar Stimulation

To compare the development of the auditory system in hearing and completely acoustically deprived animals, naive congenitally deaf white cats (CDCs) and hearing controls (HCs) were investigated at different developmental stages from birth till adulthood. The CDCs had no hearing experience before the acute experiment. In both groups of animals, responses to cochlear implant stimulation were acutely assessed. Electrically evoked auditory brainstem responses (E-ABRs) were recorded with monopolar stimulation at different current levels. CDCs demonstrated extensive development of E-ABRs, from first signs of responses at postnatal (p.n.) day 3 through appearance of all waves of brainstem response at day 8 p.n. to mature responses around day 90 p.n.. Wave I of E-ABRs could not be distinguished from the artifact in majority of CDCs, whereas in HCs, it was clearly separated from the stimulus artifact. Waves II, III, and IV demonstrated higher thresholds in CDCs, whereas this difference was not found for wave V. Amplitudes of wave III were significantly higher in HCs, whereas wave V amplitudes were significantly higher in CDCs. No differences in latencies were observed between the animal groups. These data demonstrate significant postnatal subcortical development in absence of hearing, and also divergent effects of deafness on early waves II–IV and wave V of the E-ABR.

scholarly journals Hearing Damage Induced by Blast Overpressure at Mild TBI Level in a Chinchilla Model

2020 ◽  
Vol 185 (Supplement_1) ◽  
pp. 248-255
Author(s):  
Kyle D Smith ◽  
Tao Chen ◽  
Rong Z Gan
Keyword(s):  
Auditory System ◽  
Time Course ◽  
Otoacoustic Emission ◽  
Auditory Brainstem ◽  
Distortion Product Otoacoustic Emission ◽  
Mild Tbi ◽  
Distortion Product ◽  
Blast Overpressure ◽  
Brainstem Response ◽  
Hearing Damage

Abstract Introduction The peripheral auditory system and various structures within the central auditory system are vulnerable to blast injuries, and even blast overpressure is at relatively mild traumatic brain injury (TBI) level. However, the extent of hearing loss in relation to blast number and time course of post-blast is not well understood. This study reports the progressive hearing damage measured in chinchillas after multiple blast exposures at mild TBI levels (103–138 kPa or 15–20 psi). Materials and Methods Sixteen animals (two controls) were exposed to two blasts and three blasts, respectively, in two groups with both ears plugged with foam earplugs to prevent the eardrum from rupturing. Auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) were measured in pre- and post-blasts. Immunohistochemical study of chinchilla brains were performed at the end of experiment. Results Results show that the ABR threshold and DPOAE level shifts in 2-blast animals were recovered after 7 days. In 3-blast animals, the ABR and DPOAE shifts remained at 26 and 23 dB, respectively after 14 days. Variation of auditory cortex damage between 2-blast and 3-blast was also observed in immunofluorescence images. Conclusions This study demonstrates that the number of blasts causing mild TBI critically affects hearing damage.

Fetal Central Auditory System Metabolic Response to Cochlear Implant Stimulation

2002 ◽  
Vol 127 (3) ◽  
pp. 131-137 ◽  
Author(s):  
Patrick J. Antonelli ◽  
Kenneth J. Gerhardt ◽  
Robert M. Abrams ◽  
Xinyan Huang
Keyword(s):  
Auditory System ◽  
Metabolic Activity ◽  
Glucose Utilization ◽  
Metabolic Response ◽  
Auditory Brainstem ◽  
Central Auditory System ◽  
Electrode Arrays ◽  
Fetal Sheep ◽  
Brainstem Response ◽  
Normal Controls

OBJECTIVES: The purpose of this study was to examine the effects of profound auditory deprivation and its treatment by cochlear implantation and stimulation on the metabolic activity of the central auditory system in fetal sheep. METHODS: Six ovine fetuses at 85% to 90% gestation were bilaterally deafened by kanamycin perfusion and unilaterally implanted with cochlear electrode arrays. Half of the implanted animals were stimulated with an extrauterine sound processor, and half were not. Four animals served as hearing controls. One week postoperatively, central nervous system metabolic activity was evaluated in ambient laboratory noise by quantitative autoradiography using 14C-deoxyglucose. RESULTS: Kanamycin perfusion deafened all treated animals as verified by auditory brainstem response and scanning electron microscopy. Glucose utilization in the inferior colliculus was markedly lower in deafened and unstimulated animals relative to hearing controls. Glucose utilization in implanted-stimulated animals was similar to normal controls. CONCLUSIONS: Changes in central auditory system metabolic activity associated with congenital deafness may be minimized by prompt auditory habilitation.

Evaluation of the Auditory System: An Update

1983 ◽  
Vol 92 (6) ◽  
pp. 651-656 ◽  
Author(s):  
Derald E. Brackmann ◽  
Brian D. Forquer
Keyword(s):  
Auditory System ◽  
Auditory Brainstem Response ◽  
Accurate Method ◽  
Auditory Brainstem ◽  
Impedance Audiometry ◽  
Hearing Thresholds ◽  
Behavioral Techniques ◽  
Brainstem Response ◽  
Acoustic Tumor ◽  
Auditory Brainstem Response Audiometry

The purpose of this paper is to describe the audiologic techniques currently used at the Otologic Medical Group, Inc. Auditory threshold in children is determined by a combination of behavioral and objective audiometric techniques. When behavioral techniques fail, auditory brainstem response audiometry combined with impedance audiometry gives a good estimate of hearing thresholds. Impedance audiometry is a valuable addition to the diagnosis of cochlear otosclerosis. This technique is also of benefit in the neurotologic evaluation. Auditory brainstem response audiometry is the most accurate method of detecting an acoustic tumor. We no longer use SISI, tone decay, or Bekesy tests. The newer audiometric studies have greatly improved our evaluation of the auditory system.

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