Detrimental noise effects on brain's speech functions

Background noise has become part of our everyday life in modern societies. Its presence affects both the ability to concentrate and communicate. Some individuals, like children, the elderly, and non-native speakers have pronounced problems in noisy environments. Here we review evidence suggesting that background noise has both transient and sustained detrimental effects on central speech processing. Studies on the effects of noise on neural processes have demonstrated hemispheric reorganization in speech processing in adult individuals during background noise. During noise, the well-known left hemisphere dominance in speech discrimination became right hemisphere preponderant. Furthermore, long-term exposure to noise has a persistent effect on the brain organization of speech processing and attention control. These results both stress the importance to re-evaluate which noise levels can be considered safe for brain functions and raise concerns on the speech and cognitive abilities of individuals living in noisy environments.     

Effect of baicalein from Scutellaria baicalensis on prevention of noise-induced hearing loss

Noise-induced hearing loss (NIHL) has been thought to primarily involve damage to the sensory hair cells of the cochlea via mechanical and metabolic mechanisms. This study examined the effects of baicalin, baicalein, and Scutellaria baicalensis (SB) extract against NIHL in a mouse model. Mice received oral treatment with SB, baicalin, baicalein beginning 30 min prior to noise exposure and continuing once daily throughout the study. Hearing threshold shift was assessed by auditory brain stem responses for 35 days following noise exposure. Central auditory function was evaluated by auditory middle latency responses. Cochlear function was determined based on transient evoked otoacoustic emissions. SB significantly reduced threshold shift, central auditory function damage, and cochlear function deficits, suggesting that SB may protect auditory function in NIHL and that the active constituent may be a flavonoid, baicalein.     

To modulate and be modulated: estrogenic influences on auditory processing of communication signals within a socio-neuro-endocrine framework

Gonadal hormones modulate behavioral responses to sexual stimuli, and communication signals can also modulate circulating hormone levels. In several species, these combined effects appear to underlie a two-way interaction between circulating gonadal hormones and behavioral responses to socially salient stimuli. Recent work in songbirds has shown that manipulating local estradiol levels in the auditory forebrain produces physiological changes that affect discrimination of conspecific vocalizations and can affect behavior. These studies provide new evidence that estrogens can directly alter auditory processing and indirectly alter the behavioral response to a stimulus. These studies show that: 1) Local estradiol action within an auditory area is necessary for socially relevant sounds to induce normal physiological responses in the brains of both sexes; 2) These physiological effects occur much more quickly than predicted by the classical time-frame for genomic effects; 3) Estradiol action within the auditory forebrain enables behavioral discrimination among socially relevant sounds in males; and 4) Estradiol is produced locally in the male brain during exposure to particular social interactions. The accumulating evidence suggests a socio-neuro-endocrinology framework in which estradiol is essential to auditory processing, is increased by a socially relevant stimulus, acts rapidly to shape perception of subsequent stimuli experienced during social interactions, and modulates behavioral responses to these stimuli. Brain estrogens are likely to function similarly in both songbird sexes because aromatase and estrogen receptors are present in both male and female forebrain. Estrogenic modulation of perception in songbirds and perhaps other animals could fine-tune male advertising signals and female ability to discriminate them, facilitating mate selection by modulating behaviors.     

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.     

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.     

Environmental noise-exposed workers: event-related potentials, neuropsychological and mood assessment.

Prolonged environmental noise exposure can induce pathogenic effects on various physical and psychosocial responses. The first aim of this study was to investigate whether long-term occupational noise exposure could affect neurophysiological, neuropsychological and emotional statuses, with particular respect to attention and working memory. The second aim was to evaluate the effects on the tactile P300 of a specific stressor (background traffic noise) vs a non-specific stress inductor (Stroop test). The comparison between a group of noise-exposed workers (traffic police officers), and a control group (office employees) did not show marked differences in cognitive and emotional profiles. The amplitude of the baseline cognitive potential (P300), recorded during a tactile (electric) discrimination task, resulted higher in noise-exposed workers than in controls, and this enhancement was associated with a lower level of trait anxiety and better mood profiles. Moreover, we found a wider P300 amplitude reduction in traffic police officers than in controls, under noisy conditions due to traffic. The effect of the Stroop test as a stress inductor was negligible and similar in the two groups. The wider amplitude of the non-auditory P300 in traffic police officers in the baseline condition could be a sign of cross-modal cerebral plasticity enhancing attentive processes in the 'stress-free' sensory channel. In addition, noise-exposed workers presented a higher cerebral sensitivity to stress selectively when they were exposed to the habitual environmental stressor.     

Alleles that modulate late life hearing in genetically heterogeneous mice

A genetically heterogeneous population of mice was tested for hearing at 8, 18, and 22 months by auditory brainstem response (ABR), and genotyped at 128 markers to identify loci that modulate late life hearing loss. Half of the test mice were exposed to noise for 2 hours at age 20 months. Polymorphisms affecting hearing at 18 months were noted on chromosomes 2, 3, 7, 10, and 15. Most of these loci had effects only on responses to 48 kHz stimuli, but a subset also influenced the auditory brainstem response at lower frequencies. Loci on chromosomes 4, 10, 12, and 14 had significant effects on hearing at 22 months in noise-exposed mice, and loci on chromosomes 10 and 11 had effects on mice not exposed to noise. Outer hair cell loss was modulated by polymorphisms on chromosomes 10, 11, 12, 17, and 19. Resistance to age-related hearing loss is thus modulated by a set of genetic effects, some age-specific, some frequency specific, some dependent on prior exposure to noise, and some of which compromise survival of cochlear hair cells.     

Noise-induced cell death in the mouse medial geniculate body and primary auditory cortex

Noise-induced effects within the inner ear have been well investigated for several years. However, this peripheral damage cannot fully explain the audiological symptoms in noise-induced hearing loss (NIHL), e.g. tinnitus, recruitment, reduced speech intelligibility, hyperacusis. There are few reports on central noise effects. Noise can induce an apoptosis of neuronal tissue within the lower auditory pathway. Higher auditory structures (e.g. medial geniculate body, auditory cortex) are characterized by metabolic changes after noise exposure. However, little is known about the microstructural changes of the higher auditory pathway after noise exposure. The present paper was therefore aimed at investigating the cell density in the medial geniculate body (MGB) and the primary auditory cortex (AI) after noise exposure. 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 1 week, auditory brainstem response recordings (ABR) were performed in noise exposed and normal hearing animals. After fixation, the brain was microdissected and stained (Kluever-Barrera). The cell density in the MGB subdivisions and the AI were determined by counting the cells within a grid. Noise-exposed animals showed a significant ABR threshold shift over the whole frequency range. Cell density was significantly reduced in all subdivisions of the MGB and in layers IV-VI of AI. The present findings demonstrate a significant noise-induced change of the neuronal cytoarchitecture in central key areas of auditory processing. These changes could contribute to the complex psychoacoustic symptoms after NIHL.     

From genes to behavior in developmental dyslexia

All four genes thus far linked to developmental dyslexia participate in brain development, and abnormalities in brain development are increasingly reported in dyslexia. Comparable abnormalities induced in young rodent brains cause auditory and cognitive deficits, underscoring the potential relevance of these brain changes to dyslexia. Our perspective on dyslexia is that some of the brain changes cause phonological processing abnormalities as well as auditory processing abnormalities; the latter, we speculate, resolve in a proportion of individuals during development, but contribute early on to the phonological disorder in dyslexia. Thus, we propose a tentative pathway between a genetic effect, developmental brain changes, and perceptual and cognitive deficits associated with dyslexia.     

Noise trauma impairs neurogenesis in the rat hippocampus

The hippocampus, a major site of neurogenesis in the adult brain, plays an important role in memory. Based on earlier observations where exposure to high-intensity noise not only caused hearing loss but also impaired memory function, it is conceivably that noise exposure may suppress hippocampal neurogenesis. To evaluate this possibility, nine rats were unilaterally exposed for 2 h to a high-intensity, narrow band of noise centered at 12 kHz at 126 dB SPL. The rats were also screened for noise-induced tinnitus, a potential stressor which may suppress neurogenesis. Five rats developed persistent tinnitus-like behavior while the other four rats showed no signs of tinnitus. Age-matched sham controls showed no signs of hearing loss or tinnitus. The inner ear and hippocampus were evaluated for sensory hair cell loss and neurogenesis 10 weeks post-exposure. All noise exposed rats showed severe loss of sensory hair cells in the noise-exposed ear, but essentially no damage in the unexposed ear. Frontal sections from the hippocampus were immunolabeled for doublecortin to identify neuronal precursor cells, or Ki67 to label proliferating cells. Noise-exposed rats showed a significant reduction of neuronal precursors and fewer dividing cells as compared to sham controls. However, we could not detect any difference between rats with behavioral evidence of tinnitus versus rats without tinnitus. These results show for the first time that high intensity noise exposure not only damages the cochlea but also causes a significant and persistent decrease in hippocampal neurogenesis that may contribute to functional deficits in memory.     

Post-exposure treatment with ginsenoside compound K ameliorates auditory functional injury associated with noise-induced hearing loss in mice

Noise-induced hearing loss (NIHL) is thought to primarily involve damage to the sensory hair cells of the cochlea via mechanical and metabolic mechanisms. Unfortunately, initial studies assessing the effectiveness of post-exposure treatment after hearing loss have yielded largely disappointing results. This study explored the effects of oral treatment with Korean red ginseng (RG) and with two bioavailable ginsenoside metabolites, ginsenoside Rh1 and ginsenoside compound K (GCK), in response to NIHL in a murine model. Pharmacological treatments began 24h after noise exposure and were continued once daily for 7 days. Central auditory function was evaluated using auditory middle latency responses, and cochlear function was determined based on transient evoked otoacoustic emissions. Additionally, cochlear hair cell morphology was investigated after noise exposure. Both Korean red ginseng and compound K reduced threshold shifts, central auditory function damage, and cochlear functional and morphological deficits. In contrast, treatment with ginsenoside Rh1 did not result in recovery of NIHL in mice. These results suggest that consumption of Korean red ginseng may facilitate recovery from noise-induced hearing loss. Furthermore, one of the active constituents in ginseng is likely ginsenoside compound K.     

Electrophysiological Signs of Neurocognitive Deficits in Long-Term Leukemia Survivors

The long-term effects of disease and treatment on electrophysiologicalmeasures of neurocognitive function were studied in childrenwho had survived acute lymphoblastic leukemia (ALL) for at least4 years and were currently in remission. We report here changesin cognitive processing time as shown by the latency of theP3 wave of the auditory event-related EEG potential (ERP). P3latency was significantly prolonged in long-term ALL surivors,as well as in patients successfully trreated for solid tumors(ST)outside the CNS who received similar chemotherapy but did notreceive prophylactic treatment to the CNS. P3 latencies werestrongly correlated with measures of school performance andIQ in these individuals. The similarity in P3 latency betweenthe ALL and ST groups suggests that the treatments used on thesepateints produce changes in electrophysiological responses thatare associated with mild, but significant, cognitive deficits.     

Behavioral and [F-18] fluorodeoxyglucose micro positron emission tomography imaging study in a rat chronic mild stress model of depression

We investigated changes in behavior and brain glucose metabolism in a rat chronic mild stress (CMS) model of depression. The CMS model has been used to mimic depression in humans by using various chronic mild stressors in a 4 weeks period. In the present study, we have developed a combination of tests examining behavior (open field test) and hedonic measure (sucrose preference test) after exposure to CMS, and compared this to control non-stressed rats. We found that CMS induced behavioral changes, including decreased central and rearing activity, increased grooming and defecation, reduced body weight, and reduced relative sucrose intake. Moreover, our study suggests that CMS administered for 4 weeks activated left auditory cortex, while left piriform cortex, left inferior colliculus, septal nuclei and periaqueductal gray were deactivated. These changes in region of interest are left–right asymmetrical and lateralized in the left hemisphere. And activity deficits of depression are related with changes of brain activity in all brain regions showing significant changes by CMS in glucose metabolism. There are significant correlations for relative sucrose intake in left piriform cortex, left inferior colliculus and left auditory cortex, and for anxiety-related behavioral measures in septal nuclei and periaqueductal gray. There are lack of significant effects in the mean glucose metabolism of both hemispheres in hippocampus and amygdala induced by CMS possibly because of various reasons. Changes in glucose metabolism support the view that these significant brain regions are involved in chronic stress and depressive mood regulation. The results of this study might contribute to the awareness of changes in behavior and brain activity of depression induced by CMS.     

Song system auditory responses are stable and highly tuned during sedation,rapidly modulated and unselective during wakefulness,and suppressed by arousal

We used auditory responsiveness in the avian song system to investigate the complex relationship between behavioral state and sensory processing in a high-order sensorimotor brain area. We present evidence from recordings in awake, anesthetized, and sleeping male zebra finches (Taeniopygia guttata) that auditory responsiveness in nucleus HVc is profoundly affected by changes in behavioral state. In anesthetized and sleeping birds, auditory responses were characterized by an increase in firing rate that was selective for the bird's own song (BOS) and highly stable over time. In contrast, HVc responses during wakefulness were extremely variable and transitioned between undetectable and robust levels over short intervals. Surprisingly, auditory responses in awake birds were not selective for the BOS stimulus. The variability of HVc auditory responses in awake birds suggests that, as in mammals, wakefulness is not a uniform behavioral state. Rather, auditory responsiveness likely is continually influenced by variables such as arousal state. We therefore developed several experimental paradigms in which we could manipulate arousal levels during auditory stimulus presentation. In all cases, arousal suppressed HVc auditory responses. This effect was specific to the song system, as auditory responses in Field L, a primary auditory area that is a source of auditory input to HVc, were unaffected. While arousal acts as a negative regulator of HVc auditory responsiveness, the presence and variability of the responses observed in awake, alert birds suggests that other mechanisms, such as attention, may enhance auditory responsiveness. The interplay between behavioral state and sensory processing may regulate song system responsiveness according to the bird's behavioral and social context.     

Structural changes in the adult rat auditory system induced by brief postnatal noise exposure

In previous studies (Grécová et al., Eur J Neurosci 29:1921–1930, 2009; Bures et al., Eur J Neurosci 32:155–164, 2010), we demonstrated that after an early postnatal short noise exposure (8 min 125 dB, day 14) changes in the frequency tuning curves as well as changes in the coding of sound intensity are present in the inferior colliculus (IC) of adult rats. In this study, we analyze on the basis of the Golgi–Cox method the morphology of neurons in the IC, the medial geniculate body (MGB) and the auditory cortex (AC) of 3-month-old Long–Evans rats exposed to identical noise at postnatal day 14 and compare the results to littermate controls. In rats exposed to noise as pups, the mean total length of the neuronal tree was found to be larger in the external cortex and the central nucleus of the IC and in the ventral division of the MGB. In addition, the numerical density of dendritic spines was decreased on the branches of neurons in the ventral division of the MGB in noise-exposed animals. In the AC, the mean total length of the apical dendritic segments of pyramidal neurons was significantly shorter in noise-exposed rats, however, only slight differences with respect to controls were observed in the length of basal dendrites of pyramidal cells as well as in the neuronal trees of AC non-pyramidal neurons. The numerical density of dendritic spines on the branches of pyramidal AC neurons was lower in exposed rats than in controls. These findings demonstrate that early postnatal short noise exposure can induce permanent changes in the development of neurons in the central auditory system, which apparently represent morphological correlates of functional plasticity.     

Expression of c-fos in auditory and non-auditory brain regions of the gerbil after manipulations that induce tinnitus

Subjective tinnitus is a phantom sound sensation that does not result from acoustic stimulation and is audible to the affected subject only. Tinnitus-like sensations in animals can be evoked by procedures that also cause tinnitus in humans. In gerbils, we investigated brain activation after systemic application of sodium salicylate or exposure to loud noise, both known to be reliable tinnitus-inductors. Brains were screened for neurons containing the c-fos protein. After salicylate injections, auditory cortex was the only auditory area with consistently increased numbers of immunoreactive neurons compared to controls. Exposure to impulse noise led to prolonged c-fos expression in auditory cortex and dorsal cochlear nucleus. After both manipulations c-fos expression was increased in the amygdala, in thalamic midline, and intralaminar areas, in frontal cortex, as well as in hypothalamic and brainstem regions involved in behavioral and physiological defensive reactions. Activation of these non-auditory areas was attributed to acute stress, to aversive-affective components and autonomous reactions associated with the treatments and a resulting tinnitus. The present findings are in accordance with former results that provided evidence for suppressed activation in auditory midbrain but enhanced activation of the auditory cortex after injecting high doses of salicylate. In addition, our present results provide evidence that acute stress coinciding with a disruption of hearing may evoke activation of the auditory cortex. We interpret these results in favor of our model of central tinnitus generation.     

Effects of arteether on an auditory radial-arm maze task in rats

We evaluated the behavioral and neural toxicity of the artemisinin antimalarial compound, arteether (AE), using a novel radial-arm maze procedure. We have previously shown that AE can produce a distinctive pattern of neurotoxicity in the brainstem and that auditory nuclei are particularly vulnerable. Thus, we assessed performance which depended upon auditory processing. We trained rats to choose one of eight arms of a radial maze, depending upon which arm served as the source of a white noise stimulus. Correct responses produced food reinforcement while incorrect choices had no programmed consequences. When the task was acquired, AE (25 mg/kg/day; n=7) or oil vehicle (n=7) was administered (intramuscularly) for seven consecutive days. Behavioral sessions were conducted during the days of drug administrations and for 7 days following drug administrations. Subsequently, histopathology was conducted and a quantitative assessment of the nucleus trapezoideus was made. AE produced a progressive deficit in performance on the maze task. That is, accuracy decreased, choice latency increased, and the number of trials completed decreased. Moreover, the greatest deficits were observed during the period following drug administrations. AE-treated rats revealed marked damage in the nucleus trapezoideus. The damage included chromatolysis, necrosis, and gliosis. Vehicle-treated rats did not show performance deficits or neuropathology. These results extend earlier studies and show that AE can produce damage in the n. trapezoideus of rats, which is associated with performance deficits on a complex auditory task. Thus, the auditory radial-arm maze task is a useful tool for assessing AE-induced toxicity.     

Fos-like immunoreactivity in auditory and nonauditory brain structures of hamsters previously exposed to intense sound

Fos-like immunoreactivity (FLI) was evaluated in auditory and nonauditory brain structures in hamsters that had been exposed previously to intense sound and tested behaviorally for tinnitus. The immunocytochemical results demonstrated a significant increase in exposed animals of FLI in auditory brain structures such as the lateral lemniscus, central nucleus of inferior colliculus, and auditory cortex, as well as in some nonauditory brain structures such as the locus coeruleus, lateral parabrachial nucleus, certain subregions of the hypothalamus, and amygdala. The behavioral scores suggest that animals that had been exposed to intense sound developed tinnitus. This is consistent with the hypothesis that FLI induced by intense sound exposure might represent a neural correlate of tinnitus or of plasticity associated with tinnitus. The possibility and the mechanisms underlying the increased FLI are discussed.     

Somatosensory context alters auditory responses in the cochlear nucleus

The cochlear nucleus, the first central auditory structure, performs initial stimulus processing and segregation of information into parallel ascending pathways. It also receives nonauditory inputs. Here we show in vivo that responses of dorsal cochlear nucleus (DCN) principal neurons to sounds can change significantly depending on the presence or absence of inputs from the somatosensory dorsal column nucleus occurring before the onset of auditory stimuli. The effects range from short-term suppression of spikes lasting a few milliseconds at the onset of the stimulus to long-term increases or decreases in spike rate that last throughout the duration of an acoustic stimulus (up to several hundred milliseconds). The long-term effect requires only a single electrical stimulus pulse to initiate and seems to be similar to persistent activity reported in other parts of the brain. Among the DCN inhibitory interneurons, only the cartwheel cells show a long-term rate decrease that could account for the rate increases (but not the decreases) of DCN principal cells. Thus even at the earliest stages of auditory processing, the represented information is dependent on nonauditory context, in this case somatosensory events.