Loud Noise Exposure Produces DNA, Neurotransmitter and Morphological Damage within Specific Brain Areas.
Ontology highlight
ABSTRACT:
SUBMITTER: Frenzilli G
PROVIDER: S-EPMC5483448 | biostudies-other | 2017
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Human language is supported by a cortical network involving Broca's area, which comprises Brodmann Areas 44 and 45 (BA44 and BA45). While cytoarchitectonic homolog areas have been identified in nonhuman primates, it remains unknown how these regions evolved to support human language. Here, we use histological data and advanced cortical registration methods to precisely compare the morphology of BA44 and BA45 in humans and chimpanzees. We found a general expansion of Broca's areas in humans, with the left BA44 enlarging the most, growing anteriorly into a region known to process syntax. Together with recent functional and receptorarchitectural studies, our findings support the conclusion that BA44 evolved from an action-related region to a bipartite system, with a posterior portion supporting action and an anterior portion supporting syntactic processes. Our findings add novel insights to the longstanding debate on the relationship between language and action, and the evolution of Broca's area.
| S-EPMC10501646 | biostudies-literature
Project description:Husbandry procedures and facility settings, such as low-frequency fire alarms, can produce noises in a laboratory environment that cause stress to animals used in research. However, most of the data demonstrating harmful effects that have, consequently, led to adaptations to management, have largely come from laboratory rodents with little known of the impacts on avian behavior and physiology. Here we examined whether exposure to a routine laboratory noise, a low-frequency fire alarm test, induced behavioral changes in laboratory zebra finches (Taeniopygia guttata). Twenty-four breeding pairs of zebra finches were randomly selected and exposed to the low-frequency fire alarm (sounding for 10-20 s) or no noise (control) on separate test days. All birds were filmed before and after the alarm sounded and on a control day (without the alarm). The zebra finches decreased their general activity and increased stationary and social behaviors after exposure to the alarm. Brief exposure to a low-frequency alarm disrupted the birds' behavior for at least 15 min. The induction of this behavioral stress response suggests that low-frequency sound alarms in laboratory facilities have the potential to compromise the welfare of laboratory birds.
| S-EPMC7815526 | biostudies-literature
Project description:IntroductionLoud noise-exposure can generate noise-induced tinnitus in both humans and animals. Imaging and in vivo studies show that noise exposure affects the auditory cortex; however, cellular mechanisms of tinnitus generation are unclear.MethodsHere we compare membrane properties of layer 5 (L5) pyramidal cells (PCs) and Martinotti cells expressing the cholinergic receptor nicotinic alpha 2 subunit gene (Chrna2) of the primary auditory cortex (A1) from control and noise-exposed (4-18 kHz, 90 dB, 1.5 h, followed by 1.5 h silence) 5-8 week old mice. PCs were furthermore classified in type A or type B based on electrophysiological membrane properties, and a logistic regression model predicting that afterhyperpolarization (AHP) and afterdepolarization (ADP) are sufficient to predict cell type, and these features are preserved after noise trauma.ResultsOne week after a loud noise-exposure no passive membrane properties of type A or B PCs were altered but principal component analysis showed greater separation between type A PCs from control and noise-exposed mice. When comparing individual firing properties, noise exposure differentially affected type A and B PC firing frequency in response to depolarizing current steps. Specifically, type A PCs decreased initial firing frequency in response to +200 pA steps (p = 0.020) as well as decreased steady state firing frequency (p = 0.050) while type B PCs, on the contrary, significantly increased steady state firing frequency (p = 0.048) in response to a + 150 pA step 1 week after noise exposure. In addition, L5 Martinotti cells showed a more hyperpolarized resting membrane potential (p = 0.04), higher rheobase (p = 0.008) and an increased initial (p = 8.5 × 10-5) and steady state firing frequency (p = 6.3 × 10-5) in slices from noise-exposed mice compared to control.DiscussionThese results show that loud noise can cause distinct effects on type A and B L5 PCs and inhibitory Martinotti cells of the primary auditory cortex 1 week following noise exposure. As the L5 comprises PCs that send feedback to other areas, loud noise exposure appears to alter levels of activity of the descending and contralateral auditory system.
| S-EPMC10192617 | biostudies-literature
Project description:BackgroundThere is mounting evidence that neural memory traces are formed by auditory learning in utero and that premature newborns are particularly sensitive to the intense, sustained noises or impulses sounds associated with the use of intensive care equipment. One area of critical importance is the determination of sound level exposure in utero associated with maternal occupation. The attenuation factors provided by the abdomen and tissue as well as the routes by which the inner ear receives stimulation need careful consideration and investigation to provide prenatal protection from external sound levels and frequencies that may cause harm.ObjectiveTo measure how sound from external sound sources is transmitted to the fetus inside the uterus of a pregnant sheep in 6 Hz frequency steps between 100 Hz and 20 kHz (ie, across most of the human audio range).Study designWe measured acoustic transfer characteristics in vivo in 6 time-mated singleton pregnant Romney ewes (gestational age, 103-130 days, weight, 54-74 kg). Under general anesthesia and at hysterotomy, a calibrated hydrophone was attached to the occiput of the fetal head within the amniotic sac. Two calibrated microphones were positioned in the operating theater, close to the head and to the body of each ewe. Initial experiments were carried out on 3 pregnant ewes 3 days after transport recovery to inform the data acquisition protocol. This was followed by detailed data acquisition of 3 pregnant ewes under general anesthesia, using external white noise signals. Voltage signals were acquired with 2 calibrated microphones, located near the head and the body of each ewe and with a calibrated hydrophone located in the amniotic fluid.ResultsMeasurement of acoustic transmission through the maternal abdominal and uterine walls indicates that frequency contents above 10 kHz are transmitted into the amniotic sac and that some frequencies are attenuated by as little as 3 dB.ConclusionThis study provides new data about in utero sound transmission of external noise sources beyond physiological noise (cardiovascular, respiratory, and intestinal sounds), which help quantity the potential for fetal physiological damage resulting from exposure to high levels of noise during pregnancy. Fine-frequency acoustic attenuation characteristics are essential to inform standards and clinical recommendations on exposure of pregnant women to noise. Such transfer functions may also inform the design of filters to produce an optimal acoustic setting for maternal occupational noise exposure, use of magnetic resonance imaging during pregnancy, and for neonatal incubators.
| S-EPMC7613564 | biostudies-literature
Project description:Wild-type alpha-synuclein, a protein of unknown function, has received much attention because of its involvement in a series of diseases that are known as synucleinopathies. We find that long-lasting potentiation of synaptic transmission between cultured hippocampal neurons is accompanied by an increase in the number of alpha-synuclein clusters. Conversely, suppression of alpha-synuclein expression through antisense nucleotide and knockout techniques blocks the potentiation, as well as the glutamate-induced increase in presynaptic functional bouton number. Consistent with these findings, alpha-synuclein introduction into the presynaptic neuron of a pair of monosynaptically connected cells causes a rapid and long-lasting enhancement of synaptic transmission, and rescues the block of potentiation in alpha-synuclein null mouse cultures. Also, we report that the application of nitric oxide (NO) increases the number of alpha-synuclein clusters, and inhibitors of NO-synthase block this increase, supporting the hypothesis that NO is involved in the enhancement of the number of alpha-synuclein clusters. Thus, alpha-synuclein is involved in synaptic plasticity by augmenting transmitter release from the presynaptic terminal.
| S-EPMC526467 | biostudies-literature
Project description:We present an unusual case of a patient with a positive Tullio phenomenon, brief Valsalva-induced transient horizontal nystagmus, reduced left caloric response, and bilateral vestibulo-ocular reflex loss. This study discusses the pathophysiology and differential diagnosis concerning the suspected pathology for the phenomenon of utricular hydrops or vestibular atelectasis and presents a literature review.
| S-EPMC7224419 | biostudies-literature
Project description:Cochlear inflammatory response to various environmental insults, including acoustic and ototoxic overexposures, has been increasingly become a topic of interest. As the immune response is associated with both pathology and protection, targeting specific components of the immune response is expected to dissect the relationships between cellular damage and inflammation-associated protection and repair in the cochlea. Duffy antigen receptor for chemokines (DARC) is a member of a group of atypical chemokine receptors, and essential for chemokine-regulated leukocyte/neutrophil trafficking during inflammation. Previous studies have reported that Darc deficiency alters chemokine bioavailability and leukocyte homeostasis, leading to significant anti-inflammatory effects in tissues following injury. In this study, we have used Darc knockout mice to determine the impact of a deficiency in this gene on cochlear development, as well as function in cochlea subjected to various stresses. We observed that DARC is not required for normal development of cochlear function, as evidenced by typical hearing sensitivity in juvenile Darc-KO mice, as compared to wild type (WT) C57BL/6 mice. However, Darc-KO mice exhibited improved hearing recovery after intense noise exposure when compared to wild-type. The auditory brainstem response (ABR) threshold shift between KO and WT mice was most obvious at 1-week post-noise exposure. At cochlear locations above the frequency range of the energy band of damaging noise, both hair cell survival and ribbon synapse density were improved in Darc deficient animals. In addition, the mRNA levels of some major inflammatory effectors, including Mcp-1 and Gdf15, were altered in Darc-KO mice compared to control mice at 1, 3 and 7 days post-noise exposure. These data collectively suggest that the normal Darc-dependent inflammatory response slows down the process of hearing recovery, and exacerbates cellular damage in the cochlea after noise exposure.
| S-EPMC5988871 | biostudies-literature
Project description:BACKGROUND:Exposure to both occupational and nonoccupational noise is recognized as a risk factor for noise-induced hearing loss (NIHL). Although audiologists routinely inquire regarding history of noise exposure, there are limited tools available for quantifying this history or for identifying those individuals who are at highest risk for NIHL. Identifying those at highest risk would allow hearing conservation activities to be focused on those individuals. PURPOSE:To develop a detailed, task-based questionnaire for quantifying an individual's annual noise exposure (ANE) arising from both occupational and nonoccupational sources (aim 1) and to develop a short screening tool that could be used to identify individuals at high risk of NIHL (aim 2). RESEARCH DESIGN:Review of relevant literature for questionnaire development followed by a cross-sectional descriptive and correlational investigation of the newly developed questionnaire and screening tool. STUDY SAMPLE:One hundred fourteen college freshmen completed the detailed questionnaire for estimating ANE (aim 1) and answered the potential screening questions (aim 2). An additional 59 adults participated in data collection where the accuracy of the screening tool was evaluated (aim 2). DATA COLLECTION AND ANALYSIS:In study aim 1, all participants completed the detailed questionnaire and the potential screening questions. Descriptive statistics were used to quantify participant participation in various noisy activities and their associated ANE estimates. In study aim 2, linear regression techniques were used to identify screening questions that could be used to predict a participant's estimated ANE. Clinical decision theory was then used to assess the accuracy with which the screening tool predicted high and low risk of NIHL in a new group of participants. RESULTS:Responses on the detailed questionnaire indicated that our sample of college freshmen reported high rates of participation in a variety of occupational and nonoccupational activities associated with high sound levels. Although participation rates were high, ANE estimates were below highest-risk levels for many participants because the frequency of participation in these activities was low in many cases. These data illustrate how the Noise Exposure Questionnaire (NEQ) could be used to provide detailed and specific information regarding an individual's exposure to noise. The results of aim 2 suggest that the screening tool, the 1-Minute Noise Screen, can be used to identify those participants with high- and low-risk noise exposure, allowing more in-depth assessment of noise exposure history to be targeted at those most at risk. CONCLUSIONS:The NEQ can be used to estimate an individual's ANE and the 1-Minute Noise Screen can be used to identify those participants at highest risk of NIHL. These tools allow audiologists to focus hearing conservation efforts on those individuals who are most in need of those services.
| S-EPMC5304605 | biostudies-literature
Project description:The potential effects of blast exposure on the brain health of military personnel have raised concerns and led to increased surveillance of blast exposures. Neuroimaging studies have reported white matter abnormalities in brains of service members with a history of blast exposure. However, blast effects on white matter microstructure remain poorly understood. As a novel approach to screen for white matter effects, transgenic mice that express fluorescent reporters to sensitively detect axon damage and myelin remodeling were exposed to simulated repetitive blasts (once/day on 5 consecutive days). Axons were visualized using Thy1-YFP-16 reporter mice that express yellow fluorescent protein (YFP) in a broad spectrum of neurons. Swelling along damaged axons forms varicosities that fill with YFP. The frequency and size of axonal varicosities were significantly increased in the corpus callosum (CC) and cingulum at 3 days after the final blast exposure, versus in sham procedures. CC immunolabeling for reactive astrocyte and microglial markers was also significantly increased. NG2CreER;mTmG mice were given tamoxifen (TMX) on days 2 and 3 after the final blast to induce fluorescent labeling of newly synthesized myelin membranes, indicating plasticity and/or repair. Myelin synthesis was not altered in the CC over the intervening 4 or 8 weeks after repetitive blast exposure. These experiments show the advantages of transgenic reporter mice for analysis of white matter injury that detects subtle, diffuse axon damage and the dynamic nature of myelin sheaths. These results show that repetitive low-level blast exposures produce infrequent but significant axon damage along with neuroinflammation in white matter.
| S-EPMC8127063 | biostudies-literature
Project description:PurposeThe purpose of this study was to develop a time-efficient music exposure and testing paradigm that safely creates temporary cochlear dysfunction that could be used in future temporary threshold shift (TTS) studies.MethodA 30-min audio compilation of pop rock music tracks was created. Adult volunteers with normal hearing were then exposed to this music material monaurally through headphones for 30 min at 97 dBA or 15 min at 100 dBA. Levels were measured from the ear of a manikin and are considered to provide an equivalent daily noise dose based on a 3-dB exchange. We assessed the changes in their hearing, by means of distortion product otoacoustic emission (DPOAE) testing, and standard and extended high-frequency pure-tone audiometry before and after exposure. There were 17 volunteers in total. In the first trial, eight volunteers (four females; Mdnage = 31 years [interquartile range, IQR = 4.25]) were included. Although TTS was observed in all eight participants for at least one frequency, a large variation in affected frequencies was observed. To address this issue, the audio material was further remastered to adjust levels across the different frequency bands. Fourteen adults (nine newly recruited and five from the first trial; seven females; Mdnage = 31 years [IQR = 5]) were exposed to the new material.ResultsAll but two of 17 participants presented clinically significant TTS or decrease in DPOAE amplitude in at least one frequency. Statistically significant average TTS of 7.43 dB was observed at 6 kHz. There were statistically significant average DPOAE amplitude shifts of -2.55 dB at 4 kHz, -4.97 dB at 6 kHz, and -3.14 dB at 8 kHz. No participant presented permanent threshold shift.ConclusionsA monaural music paradigm was developed and shown to induce statistically significant TTS and DPOAE amplitude shifts, without evidence of permanent loss. This realistic and time-efficient paradigm may be considered a viable option for experimental studies of temporary music-induced hearing loss.Supplemental materialhttps://doi.org/10.23641/asha.25016471.
| S-EPMC11000795 | biostudies-literature