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PubMed1995

Increased limbic system symptomatology and sensitizability of young adults with chemical and noise sensitivities.

We previously hypothesized that individual differences in (a) limbic system reactivity and (b) central nervous system sensitizability underlie vulnerability to environmental stimuli, not only in the controversial clinical condition multiple chemical sensitivity (MCS), but also in the general population. Earlier research has shown overlaps in the characteristics of persons who report noise and air pollutant sensitivities. This study assessed questionnaire responses of 897 young adult college students who reported high versus low frequency of illness from several environmental chemical odors and concomitantly high versus low sensitivity to environmental noise. Subjects who reported increased rates of illness from chemical odors with or without noise sensitivity scored significantly higher (P < 0.0001) on a measure of limbic system symptomatology derived from ictal sensory, somatic, mnemonic, and behavioral manifestations of temporal lobe epilepsy. The group rating high both for illness from chemicals and for noise sensitivity had characteristics predictive of heightened sensitizability from the animal research on time-dependent sensitization (progressive response amplification to repeated, intermittent stimuli over time): i.e., higher female to male ratio (gender risk factor), increased rates of drug abuse problems in blood relatives (genetic risk factor), trait shyness (hyperreactivity to novelty), and increased carbohydrate craving. Despite the increased family histories of drug abuse and levels of personal anxiety and depression, the chemical- and noise-sensitive group reported the lowest rates of current smoking or personal drug abuse problems and the highest frequency of illness from drinking a small amount of alcohol. Taken together, the findings suggest that limbic system dysfunction associates more with chemical than with noise sensitivity; that individuals with both chemical and noise sensitivity may be the most sensitizable subset of the population for prospective studies, and that, in their substance use patterns, young adults with both chemical and noise sensitivity are more similar to MCS patients than are their peers with chemical or noise sensitivity alone.

Adolescent↗
PubMed1985

Study on the mechanism of the appearance of noise effects.

This study was undertaken to investigate the dose-response relationship between the biological effect and noise exposure, and to consider the mechanism of the appearance of noise effects. Rats were exposed to noise at intensities of 60 dB (A), 80 dB (A) and 100 dB (A) for 240 min and examined for the change of activities of dopamine-beta-hydroxylase (DBH) in serum and adrenal glands. Plasma cyclic adenosine 3',5'-monophosphate (c-AMP) levels were also measured. Some rats were given 6-hydroxydopamine (6-OHDA) as a chemical sympathectomyzing agent 20 h before noise exposure in order to consider the mechanism of the appearance of noise effects. By noise exposure, serum DBH activity was significantly (P less than 0.01) increased at each intensity compared with the control group, but there were no remarkable changes in adrenal DBH activity. Plasma c-AMP level was also significantly elevated in response to the noise stress. When the rats, which had been pretreated with 6-OHDA, were exposed to noise with an intensity of 100 dB (A), the response of serum DBH activity was no longer observed. Therefore it is suggested that the effect due to noise exposure appears through the post-ganglionic sympathetic nerve fiber.

Adrenal Glands↗
PubMed1989

Can smoking increase attention in rapid information processing during noise? Electrocortical, physiological and behavioral effects.

This study investigated the effects of smoking on subject-paced visual rapid information processing performance (RIP) under the influence of disturbing noise. The RIP task required the subjects to detect triads of even or odd digits within a pseudorandom sequence of single digits presented on a screen. Two groups of 12 female habitual smokers who were not allowed to smoke during the last 10 h preceding the test sessions underwent two test sessions each consisting of two RIP trials separated by a smoking period (habitual cigarette) for one group and by a relaxation period without smoking for the second group. Noise disturbance was presented during the second RIP trial of one of the two sessions only. Smoking increased RIP performance, but noise failed to show any measurable effect. EEG analyzed during RIP revealed the expected noise-induced decrease in alpha power. ERP analyses showed a smoking-induced decrease in the CNV-related negativity but no noise effects. The late positive wave (LP) increased after smoking, but to a lesser extent under the noise condition. The analyses of peripheral physiological measures revealed smoking- and noise-induced heart rate acceleration and cutaneous vasoconstriction. Plasma cortisol, prolactin and HGH were also increased after the noise session. The results indicate therefore that smoking increased RIP, whereas noise failed to affect mental performance, although it produced measurable vegetative stress effects.

Adult↗
PubMed2004

Levels and influencing factors of noise pollution from small-scale industries (SSIs) in a developing country.

A study was carried out to determine levels and factors that influence noise pollution from small-scale industries (SSIs) in Dar es Salaam City Tanzania. Two sites for wood- and metalworks industries were investigated. Both sites exhibited equivalent noise levels higher than 90.0 dBA, the permissible exposure level limit for occupational noise. At a woodworks SSI, noise levels were found to correlate well with machine-use age, wood-feed speed, and wood-cut depth. Additionally, noise emanating from both types of SSIs was found to influence the level of environmental noise in the neighborhood of the SSIs. One woodworks SSI was found to have a circle of influence of about 140 m. The study concluded that SSIs present a serious source of environmental noise pollution in their neighborhoods. Noise pollution from SSIs is greatly influenced by the type of SSIs and the activities they carry out, the type and age of machines they use, their location relative to residential areas in their vicinity, and in-house noise control measures.

Developing Countries↗
PubMed2003

A review of the effects of aircraft noise on wildlife and humans, current control mechanisms, and the need for further study.

Military and civilian aircraft overflights are an issue that may impact the quality of life for millions of United States residents. Aircraft noise annoys many people worldwide and is generally thought to adversely affect some wildlife species. In light of increasing demands being placed on airspace, and because of technological improvements in acoustical testing, there is a need to reexamine the effects of aircraft noise exposure on humans and wildlife. This paper reviews past research, current laws and legislation, and presents an argument for the need to revisit the effects of aircraft noise on humans and wildlife. Some evidence suggests that noise may adversely impact wildlife and humans, however, many of the past studies were inconclusive and based on relatively small sample sizes. Given that aircraft noise abatement legislation has been enacted and because of the recent promulgation of community-based noise awareness programs, future studies should be conducted to resolve public policy problems and debates associated with aircraft noise. The need to further study the effects of aircraft noise on humans and wildlife is critical for creating sustainable land use policies near aircraft installations. Data derived from these studies will be used to create sound public policies that enhance the operational capacity of military and civilian aircraft while reducing the opportunity for human and wildlife exposure to aircraft noise.

Aircraft↗
PubMed2001

In utero and postnatal exposure of Wistar rats to low frequency/high intensity noise depletes the tracheal epithelium of ciliated cells.

Chronic exposure of men or rodents to low frequency/high intensity (LFHI) noise causes a number of systemic changes that make up the so-called vibroacoustic disease (VAD), a disorder that includes alterations of the respiratory system, namely, of its epithelial layer. We have investigated here the susceptibility of the tracheal epithelium of Wistar rats to in utero and postnatal exposure to LFHI noise by comparing its ultrastructure with that of the tracheal epithelium of control rats and of animals exposed to LFHI noise only after reaching adulthood (8 weeks of age). Scanning electron microscopy (SEM) of the inner surface of rat trachea was used to determine the relative areas covered by ciliated and non-ciliated cells. In rats that were exposed in utero and postnatally to LFHI noise, we observed that out of 100 microm(2) of tracheal epithelium only 31 +/- 14 microm(2) were covered by cilia, whereas in control rats; ciliated cells occupied an average of 60 +/- 18 microm(2) out of 100 microm(2) of the epithelium; this difference between the two groups was statistically significant (p <0.05). In rats that were exposed to LFHI noise only after reaching adulthood, cilia covered 55 +/- 22 microm(2) out of 100 microm(2) of the luminal surface of the trachea, a value that, although lower than that of controls, was not found to be statistically different. We conclude that (1) the tracheal ciliated cells are damaged by exposure of rats to LFHI noise if the animals are kept under this environmental aggression during in utero and postnatal periods; (2) tracheal ciliated cells from adult rats are more resistant to the deleterious effects of LFHI noise than pleura or lung alveolar cells that were shown before to undergo marked changes upon chronic exposure of rats to LFHI noise. These findings suggest a note of caution regarding pregnant women and young children: they should be prevented from areas where LFHI noise occurs, namely, in aircraft and textile industries where this type of environmental hazard is often present.

Animals↗
PubMed2006

Evaluation of traffic noise pollution in Amman, Jordan.

The City of Amman, Jordan, has been subjected to persistent increase in road traffic due to overall increase in prosperity, fast development and expansion of economy, travel and tourism. This study investigates traffic noise pollution in Amman. Road traffic noise index L10(1 h) was measured at 28 locations that cover most of the City of Amman. Noise measurements were carried out at these 28 locations two times a day for a period of one hour during the early morning and early evening rush hours, in the presence and absence of a barrier. The Calculation of Road Traffic Noise (CRTN) prediction model was employed to predict noise levels at the locations chosen for the study. Data required for the model include traffic volume, speed, percentage of heavy vehicles, road surface, gradient, obstructions, distance, noise path, intervening ground, effect of shielding, and angle of view. The results of the investigation showed that the minimum and the maximum noise levels are 46 dB(A) and 81 dB(A) during day-time and 58 dB(A) and 71 dB(A) during night-time. The measured noise level exceeded the 62 dB(A) acceptable limit at most of the locations. The CTRN prediction model was successful in predicting noise levels at most of the locations chosen for this investigation, with more accurate predictions for night-time measurements.

Jordan↗
PubMed1987

Acute exposure to noise affects sodium-dependent high-affinity choline uptake in the central nervous system of the rat.

Rats were acutely (45 min) exposed to white noise at intensity of either 70 or 100 dB. Sodium-dependent high-affinity choline uptake was determined in the striatum, frontal cortex, hypothalamus, and hippocampus immediately after exposure. The effects of noise on choline uptake varied according to the intensity of the noise and the brain area studied. Exposure to noise of 70 dB significantly increased the choline uptake in the frontal cortex, hypothalamus, and hippocampus as compared to the uptake of sham-exposed rats, whereas decreased choline uptake in the frontal cortex and hippocampus was observed acute exposure to noise of 100 dB. No significant effect on choline uptake in the striatum was seen after exposure to noise of either intensity. In addition, pretreatment of the rats with the narcotic antagonist naltrexone (1 mg/kg, IP) before noise exposure blocked the effects of noise on choline uptake in the central nervous system. Changes in cholinergic activity in the central nervous system could be a response to the stress effect of noise and may be mediated by endogenous opioids.

Animals↗
PubMed1982

Noise impairment in the guinea pig. II. Changes of single unit responses in the inferior colliculus.

Spontaneous and evoked activity of neurons in the inferior colliculus of guinea pigs was recorded before and after exposure to noise (continuous or intermittent white noise, 115 dB SPL for 30 min). A single unit was investigated in each animal, and its activity was monitored for several hours. Exposure to noise elevated the threshold of the tip of the tuning curve, resulting in a broadening of the tuning curve. Threshold elevation at the characteristic frequency was greater after exposure to intermittent noise (200 ms noise and 200 ms pause), reaching values of 22.8 +/- 3.7 dB (means +/- S.E.) than it was after exposure to continuous noise (threshold elevation of 13.1 +/- 1.7 dB). The average threshold shift was 17.1 +/- 2 dB. Neither the shape of the poststimulus histograms nor the slope of the spike-intensity curves changed with the noise exposure. The total number of spikes during the response was, however, reduced, and the reduction was in proportion to the threshold elevation. Monaural noise exposure had no effect on the neuronal activity evoked by stimulation of the opposite, nonexposed ear. The latencies of responses recorded after exposure to noise were also longer than the latencies at the same absolute intensity recorded before the exposure. Thus the latencies during the original pre-exposure and acquired postexposure thresholds were practically identical.

Action Potentials↗
PubMed1988

Potentiation of noise induced threshold shifts and hair cell loss by carbon monoxide.

Previous studies have determined that severe systemic hypoxia disrupts cochlear function acutely, but have suggested that augmentation of cochlear perfusion may successfully protect cochlear function under all but the most profound hypoxic treatments. In the current study we report on the chronic effects of simultaneous exposures to noise and carbon monoxide on pure tone thresholds and hair cell survival in rats. Following initial threshold determination, rats received acute exposure to carbon monoxide, noise, or both agents concurrently. Thresholds were evaluated 2-4 and 6-8 weeks later. The data show that carbon monoxide alone does not affect either auditory thresholds or compromise hair cells at the light microscopic level. The noise exposure alone produced variable, but quite limited permanent threshold shifts which were related to the power spectrum of the broad band noise that was employed. Hair cell loss was restricted to the basal turn of the cochlea. Simultaneous exposure to carbon monoxide and noise induced large threshold shifts at all frequencies studied, but the effect was greatest at the highest test frequency; an effect not consistent with the noise power spectrum. Widespread hair cell loss persisted over fully half of the basilar membrane in the most severely affected rat. Outer hair cells appear to be particularly vulnerable. Carbon monoxide plus noise did not appear to preferentially disrupt a particular row of outer hair cells. These data complement existing evidence that hyperoxia can mitigate against noise induced injury and reinforce the view that some types of noise induced damage may result from metabolic insufficiencies.

Acoustic Stimulation↗
PubMed1994

The effect of 'conditioning' exposures on hearing loss from impulse noise.

Research has shown that prior noise exposures or 'conditioning' can moderate the amount of permanent threshold shift (PTS) from subsequent high intensity noise exposures. The aim of this experiment was to study the effect of 'conditioning' on subsequent exposure to high intensity impulse noise. The subjects were seven experimental and 14 control monaural chinchillas. Evoked potential (EVP) thresholds were measured before and after the noise exposures. Experimental animals received 10 days of exposure to an octave band noise (OBN) centered at 0.5 kHz OBN at 95 dB SPL (6 h on/18 h off) and allowed to recover for 5 days. The subjects were then exposed to an impulse noise at 150 dB SPL. The temporal spacing of the impulses consisted of a series of 50 pairs of impulses presented 50 ms apart with 1000 ms between the onset of each pair. The total duration of exposure was approximately 1 min. Control animals received only the impulse noise exposure. PTS was measured after 4 weeks. The threshold shift (TS) patterns during the 'conditioning' phase were consistent with previous research, with the greatest amount of TS occurring on the second day and decreasing with continued exposures. Four weeks after recovery from the impulse noise, the experimental animals showed significantly less PTS than the control animals. In addition, histological examination revealed significantly less hair cell loss in the experimental than in the control subjects. The results are discussed in the context of previous studies on 'toughening' and on the effects of impulse noise.

Acoustic Stimulation↗
PubMed1995

Noise exposure alters the response of outer hair cells to ATP.

The outer hair cells (OHCs) are one target of noise-induced effects. To date there are few studies which examine changes in the function of OHCs induced by noise exposure. There is increasing evidence that ATP may be a neuromodulator acting on OHCs. Therefore, we examined the possibility that the response to ATP may be altered by low-level noise exposure. ATP was tested on cation currents recorded from outer hair cells (OHCs) isolated from chronic noise-exposed guinea pigs and compared to currents recorded from normal control animals. The whole-cell variant of the patch-clamp technique was used. The incidence of response to 100 microM ATP was decreased in OHCs from noise-exposed animals as compared to controls when normal internal and external solutions were employed. When K+ was substituted by N-methyl-glucamine (NMG+) in the pipette solution, there were significant differences in the magnitudes of ATP-evoked currents between cells from noise-exposed and control animals. This was observed in both normal and 20 mM Ba2+ external solutions. In addition, the response to ATP exhibited a dependency on OHC length. In short OHCs (< 65 microns) from noise-exposed animals the magnitude of the response to ATP was significantly reduced. By contrast, the response in long OHCs (> 65 microns) from noise-exposed animals was increased. Results suggest that low-level noise exposure induces changes in OHCs which affect the response of the cell to ATP.

Acoustic Stimulation↗
PubMed2004

The combined effects of forward masking by noise and high click rate on monaural and binaural human auditory nerve and brainstem potentials.

OBJECTIVE: To study effects of forward masking and rapid stimulation on human monaurally- and binaurally-evoked brainstem potentials and suggest their relation to synaptic fatigue and recovery and to neuronal action potential refractoriness. METHODS: Auditory brainstem evoked potentials (ABEPs) were recorded from 12 normally- and symmetrically hearing adults, in response to each click (50 dB nHL, condensation and rarefaction) in a train of nine, with an inter-click interval of 11 ms, that followed a white noise burst of 100 ms duration (50 dB nHL). Sequences of white noise and click train were repeated at a rate of 2.89 s(-1). The interval between noise and first click in the train was 2, 11, 22, 44, 66 or 88 ms in different runs. ABEPs were averaged (8000 repetitions) using a dwell time of 25 micros/address/channel. The binaural interaction components (BICs) of ABEPs were derived and the single, centrally located equivalent dipoles of ABEP waves I and V and of the BIC major wave were estimated. RESULTS: The latencies of dipoles I and V of ABEP, their inter-dipole interval and the dipole magnitude of component V were significantly affected by the interval between noise and clicks and by the serial position of the click in the train. The latency and dipole magnitude of the major BIC component were significantly affected by the interval between noise and clicks. Interval from noise and the click's serial position in the train interacted to affect dipole V latency, dipole V magnitude, BIC latencies and the V-I inter-dipole latency difference. Most of the effects were fully apparent by the first few clicks in the train, and the trend (increase or decrease) was affected by the interval between noise and clicks. CONCLUSIONS: The changes in latency and magnitude of ABEP and BIC components with advancing position in the click train and the interactions of click position in the train with the intervals from noise indicate an interaction of fatigue and recovery, compatible with synaptic depletion and replenishing, respectively. With the 2 ms interval between noise and the first click in the train, neuronal action potential refractoriness may also be involved.

Acoustic Stimulation↗
PubMed2004

Quantitative analysis of apoptotic and necrotic outer hair cells after exposure to different levels of continuous noise.

We have reported that by 2 days after noise exposure the size of cochlear lesion was expanding by outer hair cells (OHCs) dying either by apoptosis or necrosis. The current study was designed to compare the prevalence of the two cell death pathways as a function of time after exposure to noises of different levels. Chinchillas were exposed to a narrow band noise at either 104 or 108 dB SPL for 1 h. At three time points (1, 4 and 30 days) after the noise exposure, the numbers of missing, apoptotic and necrotic OHCs in the cochleas were identified and documented with a combination of TUNEL, caspase-3 and propidium iodide labeling. The subjects exposed to the 108-dB noise showed significantly more apoptotic OHCs than necrotic OHCs in the cochleas examined at days 1 and 4 after the noise exposure. By day 30, apoptotic and necrotic pathologies continued, although in small quantity, with no significant difference in quantity between two types of cell death. The subjects exposed to the 104-dB noise showed a significant difference in the numbers of apoptotic and necrotic OHCs at day 1 after the noise exposure, whereas the difference became statistically insignificant at day 4 and day 30 after the noise exposure. The results of the study indicate that the early expansion of cochlear lesion is attributed primarily to apoptosis, whereas the later stage of lesion expansion is likely the result of an equal contribution from apoptosis and necrosis.

Animals↗
PubMed2005

Mechanisms of noise-induced hearing loss potentiation by hypoxia.

Potentiation of noise-induced permanent threshold shift (PTS) by hypoxia has been reported [Hear. Res. 172 (1-2) (2002) 186]. In this study in rats, effects of noise (110 dB SPL), hypoxia (10% O(2)), and their combination have been determined on different cochlear potentials and on the expression of genes coding proteins in the outer hair cell (OHC) membrane skeleton (beta-actin) and in the mitochondrial respiratory chain (SDHa & b). The noise exposure alone caused CAP threshold shift only in the noise-band. The combined exposure to noise and hypoxia caused an about 40-dB PTS at all frequencies within and above the noise band. Loss of the cochlear amplification was not always related to the CM-suppression. SP was only affected at high frequencies by the combined exposure. Gene expression of beta-actin was up-regulated by the noise exposure, which was blocked by hypoxia. Gene expression of SDHa was also up-regulated by the noise and the combined exposure. The data suggest that loss of the cochlear active process, due to damage to the OHC membrane skeleton and to the cellular energy generation system, is related to the noise-induced hearing loss potentiation by hypoxia. Inner hair cell damage may also be involved in the hypoxia potentiation in the basal turn.

Actins↗
PubMed2006

Personal noise ranking of road traffic: subjective estimation versus physiological parameters under laboratory conditions.

OBJECTIVE: To evaluate the subjective estimation of noise-induced discomfort and its correlation to psychoacoustic and physiological parameters under laboratory conditions. To establish an effective description of sound qualities of road traffic noise, supplementing the current standards and calculation specifications. METHODS: Pass-by vehicle noise samples were binaurally recorded with a dummy head measurement system, and synthetically composed to six vehicle ensembles considering different road beds, varying speed profiles and noise barriers. Fifty-one persons were selected and tested under laboratory conditions. Study participants were exposed to defined acoustic stimuli, alternating with neutral phases lacking acoustic content in a listening room. Concomitant recording of electrocardiogram (ECG) and respiratory rate was performed. Subjective estimation of noise-induced discomfort of assigned vehicle ensembles was rated on a personal ranking scale (PRS) by the study subjects. Subjective ratings were combined with objective psychoacoustic parameters by multiple regression analysis. RESULTS: Heart rate was increased during all noise exposure phases compared to neutral phases; the increase of heart rate differed among vehicle ensembles and was statistically significant in two cases (p<0.01). Respiratory rate remained unaffected. Personal rankings also differed among vehicle ensembles and correlated well with objective psychoacoustic parameters (p<0.0001); e.g., loudness combined with roughness describes the correlation with subjective estimation of noise-induced discomfort better than the A-weighted sound level. Vehicle ensembles rated more unpleasant caused higher increases in heart rate as well (p<0.0001). CONCLUSIONS: The sound quality of road traffic noise as it is described by various psychoacoustic parameters not only determines the subjective estimation of noise-induced discomfort but in addition affects physiological parameters like heart rate. This should be considered for future perspectives in road- and traffic planning and therefore may serve construction engineers as well as traffic planner as a supplemental tool.

Austria↗
PubMed2004

Noise-induced changes of neuronal spontaneous activity in mice inferior colliculus brain slices.

The inferior colliculus (IC) in vivo is reportedly subject to a noise-induced decrease of GABA-related inhibitory synaptic transmission accompanied by an amplitude increase of auditory evoked responses, a widening of tuning curves and a higher neuronal discharge rate at suprathreshold levels. However, other in vivo experiments which demonstrated constant neuronal auditory thresholds or unchanged spontaneous activity in the IC after noise exposure did not confirm those findings. Perhaps this can be the result of complex noise-induced interactions between different central auditory structures. It was, therefore, the aim of the present study to investigate the effects of noise exposure on the spontaneous electrical activity of single neurons in a slice preparation of the isolated mouse IC. Normal hearing mice were exposed to noise (10 kHz center frequency at 115 dB SPL for 3 h) at the age of 21 days under anesthesia (Ketamin/Rompun 10:1). After one week, auditory brainstem response (ABR) recordings and extracellular single-unit recordings from spontaneously active neurons within the IC slice were performed in noise-exposed and in normal hearing control mice. Noise-exposed animals showed a significant ABR threshold shift in the whole tested frequency range and a significant lower neuronal spontaneous activity in all investigated isofrequency laminae compared to controls. In both groups, the firing rate of 80% of IC neurons (approximately) increased significantly during the application of the GABA(A) receptor antagonist Bicucullin (10 microM). The present findings demonstrate a noise-related modulation of spontaneous activity in the IC, which possibly contribute to the generation of noise-induced tinnitus and hearing loss.

Acoustic Stimulation↗
PubMed2005

Erratum to "Noise-induced changes of neuronal spontaneous activity in mice inferior colliculus brain slices".

The inferior colliculus (IC) in vivo is reportedly subject to a noise-induced decrease of GABA-related inhibitory synaptic transmission accompanied by an amplitude increase of auditory evoked responses, a widening of tuning curves and a higher neuronal discharge rate at suprathreshold levels. However, other in vivo experiments which demonstrated constant neuronal auditory thresholds or unchanged spontaneous activity in the IC after noise exposure did not confirm those findings. Perhaps this can be the result of complex noise-induced interactions between different central auditory structures. It was, therefore, the aim of the present study to investigate the effects of noise exposure on the spontaneous electrical activity of single neurons in a slice preparation of the isolated mouse IC. Normal hearing mice were exposed to noise (10 kHz center frequency at 115 dB SPL for 3 h) at the age of 21 days under anesthesia (Ketamin/Rompun 10:1). After one week, auditory brainstem response (ABR) recordings and extracellular single-unit recordings from spontaneously active neurons within the IC slice were performed in noise-exposed and in normal hearing control mice. Noise-exposed animals showed a significant ABR threshold shift in the whole tested frequency range and a significant lower neuronal spontaneous activity in all investigated isofrequency laminae compared to controls. In both groups, the firing rate of 80% of IC neurons (approximately) increased significantly during the application of the GABA(A) receptor antagonist Bicucullin (10 microM). The present findings demonstrate a noise-related modulation of spontaneous activity in the IC, which possibly contribute to the generation of noise-induced tinnitus and hearing loss.

Acoustic Stimulation↗