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Proceedings of the National Academy of... Sep 2013Noise-induced hearing loss (NIHL) is a growing health issue, with costly treatment and lost quality of life. Here we establish Drosophila melanogaster as an inexpensive,...
Noise-induced hearing loss (NIHL) is a growing health issue, with costly treatment and lost quality of life. Here we establish Drosophila melanogaster as an inexpensive, flexible, and powerful genetic model system for NIHL. We exposed flies to acoustic trauma and quantified physiological and anatomical effects. Trauma significantly reduced sound-evoked potential (SEP) amplitudes and increased SEP latencies in control genotypes. SEP amplitude but not latency effects recovered after 7 d. Although trauma produced no gross morphological changes in the auditory organ (Johnston's organ), mitochondrial cross-sectional area was reduced 7 d after exposure. In nervana 3 heterozygous flies, which slightly compromise ion homeostasis, trauma had exaggerated effects on SEP amplitude and mitochondrial morphology, suggesting a key role for ion homeostasis in resistance to acoustic trauma. Thus, Drosophila exhibit acoustic trauma effects resembling those found in vertebrates, including inducing metabolic stress in sensory cells. This report of noise trauma in Drosophila is a foundation for studying molecular and genetic sequelae of NIHL.
Topics: Acoustic Stimulation; Animals; Behavior, Animal; Disease Models, Animal; Drosophila melanogaster; Hearing Loss, Noise-Induced; Locomotion; Microscopy, Electron, Transmission; Mitochondrial Size; Neurons; Stress, Physiological
PubMed: 24003166
DOI: 10.1073/pnas.1307294110 -
Noise & Health 2018Noise exposure, the main cause of hearing loss in countries with lot of industries, may result both in temporary or permanent hearing loss. The goal of this study was to...
INTRODUCTION
Noise exposure, the main cause of hearing loss in countries with lot of industries, may result both in temporary or permanent hearing loss. The goal of this study was to investigate the effects of parenteral papaverine and piracetam administration following an acoustic trauma on hearing function with histopathologic correlation.
MATERIALS AND METHODS
Eighteen Wistar albino rats exposed to noise for 8 h in a free environment were included. We divided the study population into three groups, and performed daily intraperitoneal injections of papaverine, piracetam, and saline, respectively, throughout the study. We investigated the histopathologic effects of cellular apoptosis on inner hair cells (IHCs) and outer hair cells (OHCs) and compared the distortion product otoacoustic emissions (DPOAEs) thresholds among the groups.
RESULTS AND DISCUSSION
On the 3 and 7 days, DPOAE thresholds at 8 kHz were significantly higher both in papaverine and piracetam groups compared with the control group (P = 0.004 for 3 day, P = 0.016 and P = 0.028 for 7 day, respectively). On the 14 day, piracetam group had significantly higher mean thresholds at 8 kHz (P = 0.029); however, papaverine group had similar mean thresholds compared to the control group (P = 0.200). On the 3 and 7 days following acoustic trauma, both IHC and OHC loss were significantly lower in both papaverine and piracetam groups. On the 7 day, the mean amount of apoptotic IHCs and OHCs identified using Caspase-3 method were significantly lower in both groups, but the mean amount identified using terminal deoxynucleotidyl transferase dUTP nick end labeling method were similar in both groups compared to the control group.
CONCLUSION
We demonstrated the effects of papaverine and piracetam on the recovery of cochlear damage due to acoustic trauma on experimental animals using histopathologic and electrophysiologic examinations.
Topics: Animals; Apoptosis; Electrophysiology; Hair Cells, Auditory, Inner; Hair Cells, Auditory, Outer; Hearing Loss, Noise-Induced; Injections, Intraperitoneal; Male; Neuroprotective Agents; Otoacoustic Emissions, Spontaneous; Papaverine; Piracetam; Rats, Wistar
PubMed: 29676295
DOI: 10.4103/nah.NAH_31_17 -
Magnesium Research Dec 2006Acoustic trauma is one of the major causes of hearing loss and tinnitus, particularly in industrial environments. Noise-induced hearing loss (NIHL) results in direct... (Review)
Review
Acoustic trauma is one of the major causes of hearing loss and tinnitus, particularly in industrial environments. Noise-induced hearing loss (NIHL) results in direct mechanical damage as well as in indirect metabolic processes. Metabolic disorders have multiple origins: ionic, ischemic, excitotoxic and production of cochlear free radicals causing cell death, due to necrosis or apoptosis. The efficacy of magnesium, administered either to prevent or to treat NIHL has been demonstrated in several studies in animals and in humans. Magnesium, which easily crosses the hematocochlear barrier, presents neuroprotective and vasodilatory effects, and thus, is able to limit the cochlear damage. Magnesium therapy is well documented because it is usually prescribed in other pathologies. Its side effects and contraindications are few and it is cheap. This article presents also some arguments that emphasize the interest of magnesium therapy in acoustic trauma.
Topics: Animals; Cochlea; Free Radicals; Guinea Pigs; Hearing Loss, Noise-Induced; Humans; Ion Channels; Ischemia; Magnesium; Microscopy, Electron, Scanning; Oxidative Stress
PubMed: 17402292
DOI: No ID Found -
The American Journal of Pathology Sep 2020Acoustic trauma disrupts cochlear blood flow and damages sensory hair cells. Damage and regression of capillaries after acoustic trauma have long been observed, but the...
Acoustic Trauma Causes Cochlear Pericyte-to-Myofibroblast-Like Cell Transformation and Vascular Degeneration, and Transplantation of New Pericytes Prevents Vascular Atrophy.
Acoustic trauma disrupts cochlear blood flow and damages sensory hair cells. Damage and regression of capillaries after acoustic trauma have long been observed, but the underlying mechanism of pathology has not been understood. We show herein that loud sound causes change of phenotype from neural/glial antigen 2 positive/α-smooth muscle actin negative to neural/glial antigen 2 positive/α-smooth muscle actin positive in some pericytes (PCs) on strial capillaries that is strongly associated with up-regulation of transforming growth factor-β1. The acoustic trauma also reduced capillary density and increased deposition of matrix proteins, particularly in the vicinity of transformed PCs. In a newly established in vitro three-dimensional endothelial cell (EC) and PC co-culture model, transformed PCs induced thicker capillary-like branches in ECs and increased collagen IV and laminin expression. Transplantation of exogenous PCs derived from neonatal day 10 mouse cochleae to acoustic traumatized cochleae, however, significantly attenuated the decreased vascular density in the stria. Transplantation of PCs pretransfected with adeno-associated virus 1-vascular endothelial growth factor-A165 under control of a hypoxia-response element markedly promotes vascular volume and blood flow, increased proliferation of PCs and ECs, and attenuated loud sound-caused loss in endocochlear potential and hearing. Our results indicate that loud sound-triggered PC transformation contributes to capillary wall thickening and regression, and young PC transplantation effectively rehabilitates the vascular regression and improves hearing.
Topics: Animals; Atrophy; Capillaries; Cell Transdifferentiation; Cochlea; Hearing Loss, Noise-Induced; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Myofibroblasts; Pericytes
PubMed: 32562655
DOI: 10.1016/j.ajpath.2020.05.019 -
The Journal of the Acoustical Society... Nov 2019Rats make excellent models for the study of medical, biological, genetic, and behavioral phenomena given their adaptability, robustness, survivability, and intelligence.... (Review)
Review
Rats make excellent models for the study of medical, biological, genetic, and behavioral phenomena given their adaptability, robustness, survivability, and intelligence. The rat's general anatomy and physiology of the auditory system is similar to that observed in humans, and this has led to their use for investigating the effect of noise overexposure on the mammalian auditory system. The current paper provides a review of the rat model for studying noise-induced hearing loss and highlights advancements that have been made using the rat, particularly as these pertain to noise dose and the hazardous effects of different experimental noise types. In addition to the traditional loss of auditory function following acoustic trauma, recent findings have indicated the rat as a useful model in observing alterations in neuronal processing within the central nervous system following noise injury. Furthermore, the rat provides a second animal model when investigating noise-induced cochlear synaptopathy, as studies examining this in the rat model resemble the general patterns observed in mice. Together, these findings demonstrate the relevance of this animal model for furthering the authors' understanding of the effects of noise on structural, anatomical, physiological, and perceptual aspects of hearing.
Topics: Acoustic Stimulation; Animals; Auditory Pathways; Disease Models, Animal; Hearing Loss, Noise-Induced; Rats
PubMed: 31795685
DOI: 10.1121/1.5132553 -
Journal of Neurophysiology Apr 2016Exposure to loud sounds damages the auditory periphery and induces maladaptive changes in central parts of the auditory system. Diminished peripheral afferentation and...
Exposure to loud sounds damages the auditory periphery and induces maladaptive changes in central parts of the auditory system. Diminished peripheral afferentation and altered inhibition influence the processing of sounds in the auditory cortex. It is unclear, however, which types of inhibitory interneurons are affected by acoustic trauma. Here we used single-unit electrophysiological recording and two-photon calcium imaging in anesthetized mice to evaluate the effects of acute acoustic trauma (125 dB SPL, white noise, 5 min) on the response properties of neurons in the core auditory cortex. Electrophysiological measurements suggested the selective impact of acoustic trauma on inhibitory interneurons in the auditory cortex. To further investigate which interneuronal types were affected, we used two-photon calcium imaging to record the activity of neurons in cortical layers 2/3 and 4, specifically focusing on parvalbumin-positive (PV+) and somatostatin-positive (SST+) interneurons. Spontaneous and pure-tone-evoked firing rates of SST+ interneurons increased in layer 4 immediately after acoustic trauma and remained almost unchanged in layer 2/3. Furthermore, PV+ interneurons with high best frequencies increased their evoked-to-spontaneous firing rate ratios only in layer 2/3 and did not change in layer 4. Finally, acoustic trauma unmasked low-frequency excitatory inputs only in layer 2/3. Our results demonstrate layer-specific changes in the activity of auditory cortical inhibitory interneurons within minutes after acoustic trauma.
Topics: Action Potentials; Animals; Auditory Cortex; Evoked Potentials, Auditory; Hearing Loss, Noise-Induced; Interneurons; Mice; Mice, Inbred C57BL; Parvalbumins; Somatostatin
PubMed: 26823513
DOI: 10.1152/jn.00810.2015 -
The Journal of International Advanced... Mar 2022To investigate the possible protective activity of oleuropein compound on noise-induced hearing loss in rats.
BACKGROUND
To investigate the possible protective activity of oleuropein compound on noise-induced hearing loss in rats.
METHODS
Twenty-eight adult male albino rats were divided into 4 groups. Control normal saline (n=7) group was kept noise-free. Control oleuropein group (n=7) group was kept noise-free and was administered with 50 mg/kg/day oleuropein. The experimental normal saline (n=7) group was subjected to noise. The experimental oleuropein (n=7) group was subjected to noise and was administered with 50 mg/kg/day oleuropein. The experimental groups were subjected to 4 kHz octave noise with a frequency of 120 dB Sound Pressure Level (SPL) for 4 hours. Hearing level measurements were performed with auditory brainstem response and distortion-product otoacoustic emission tests before and after the 1st, 7th, and 10th day of the noise exposure. On the 10th day, rats were sacrificed. The temporal bones of the rats were removed and the cochlea and spiral ganglion cells were evaluated using hematoxylin-eosin staining under light microscopy.
RESULTS
Better hearing thresholds were achieved in the experimental oleuropein group compared to the experimental normal saline group at 8 kHz, 12 kHz, 16 kHz, and 32 kHz frequencies (P < .05). Although no statistically significant difference was found between the groups, in the experimental normal saline group, the percentage of damaged spiral ganglion cells was higher than the experimental oleuropein group.
CONCLUSION
Our findings suggest that oleuropein may have a partial protective effect against noise-related hearing loss. However, further research with higher doses is needed to justify this protective effect.
Topics: Animals; Auditory Threshold; Cochlea; Evoked Potentials, Auditory, Brain Stem; Hearing Loss, Noise-Induced; Iridoid Glucosides; Male; Otoacoustic Emissions, Spontaneous; Rats; Saline Solution
PubMed: 35418359
DOI: 10.5152/iao.2022.20009 -
Hearing Research Jun 2017
Topics: Auditory Pathways; Auditory Perception; Hearing; Hearing Loss, Noise-Induced; Humans; Military Medicine; Military Personnel; Noise, Occupational; Occupational Exposure; Occupational Injuries; Tinnitus
PubMed: 28526261
DOI: 10.1016/j.heares.2017.04.010 -
Expert Opinion on Investigational Drugs Jan 2017Noise-induced hearing loss (NIHL) due to industrial, military, and recreational noise exposure is a major, but also potentially preventable cause of acquired hearing... (Review)
Review
Noise-induced hearing loss (NIHL) due to industrial, military, and recreational noise exposure is a major, but also potentially preventable cause of acquired hearing loss. For the United States it is estimated that 26 million people (15% of the population) between the ages of 20 and 69 have a high-frequency NIHL at a detriment to the quality of life of the affected individuals and great economic cost to society. Areas covered: This review outlines the pathology and pathophysiology of hearing loss as seen in humans and animal models. Results from molecular studies are presented that have provided the basis for therapeutic strategies successfully applied to animals. Several compounds emerging from these studies (mostly antioxidants) are now being tested in field trials. Expert opinion: Although no clinically applicable intervention has been approved yet, recent trials are encouraging. In order to maximize protective therapies, future work needs to apply stringent criteria for noise exposure and outcome parameters. Attention needs to be paid not only to permanent NIHL due to death of sensory cells but also to temporary effects that may show delayed consequences. Existing results combined with the search for efficacious new therapies should establish a viable treatment within a decade.
Topics: Adult; Aged; Animals; Antioxidants; Hearing Loss, Noise-Induced; Humans; Middle Aged; Quality of Life; Time Factors; Young Adult
PubMed: 27918210
DOI: 10.1080/13543784.2017.1269171 -
Hearing Research Mar 2024Chronic tinnitus is a debilitating condition with very few management options. Acoustic trauma that causes tinnitus has been shown to induce neuronal hyperactivity in...
Chronic tinnitus is a debilitating condition with very few management options. Acoustic trauma that causes tinnitus has been shown to induce neuronal hyperactivity in multiple brain areas in the auditory pathway, including the inferior colliculus. This neuronal hyperactivity could be attributed to an imbalance between excitatory and inhibitory neurotransmission. However, it is not clear how the levels of neurotransmitters, especially neurotransmitters in the extracellular space, change over time following acoustic trauma and the development of tinnitus. In the present study, a range of amino acids were measured in the inferior colliculus of rats during acoustic trauma as well as at 1 week and 5 months post-trauma using in vivo microdialysis and high-performance liquid chromatography. Amino acid levels in response to sound stimulation were also measured at 1 week and 5 months post-trauma. It was found that unilateral exposure to a 16 kHz pure tone at 115 dB SPL for 1 h caused immediate hearing loss in all the animals and chronic tinnitus in 58 % of the animals. Comparing to the sham condition, extracellular levels of GABA were significantly increased at both the acute and 1 week time points after acoustic trauma. However, there was no significant difference in any of the amino acid levels measured between sham, tinnitus positive and tinnitus negative animals at 5 months post-trauma. There was also no clear pattern in the relationship between neurochemical changes and sound frequency/acoustic trauma/tinnitus status, which might be due to the relatively poorer temporal resolution of the microdialysis compared to electrophysiological responses.
Topics: Rats; Animals; Hearing Loss, Noise-Induced; Tinnitus; Acoustic Stimulation; Amino Acids; Inferior Colliculi; Neurotransmitter Agents
PubMed: 38219615
DOI: 10.1016/j.heares.2024.108948