Dataset Information

Evidence of Hyperacusis in Adult Rats Following Non-traumatic Sound Exposure.

ABSTRACT: Manipulations that enhance neuroplasticity may inadvertently create opportunities for maladaptation. We have previously used passive exposures to non-traumatic white noise to open windows of plasticity in the adult rat auditory cortex and induce frequency-specific functional reorganizations of the tonotopic map. However, similar reorganizations in the central auditory pathway are thought to contribute to the generation of hearing disorders such as tinnitus and hyperacusis. Here, we investigate whether noise-induced reorganizations are accompanied by electrophysiological or behavioral evidence of tinnitus or hyperacusis in adult Long-Evans rats. We used a 2-week passive exposure to moderate-intensity (70 dB SPL) broadband white noise to reopen a critical period for spectral tuning such that a second 1-week exposure to 7 kHz tone pips produced an expansion of the 7 kHz frequency region in the primary auditory cortex (A1). We demonstrate for the first time that this expansion also takes place in the ventral auditory field (VAF). Sound exposure also led to spontaneous and sound-evoked hyperactivity in the anterior auditory field (AAF). Rats were assessed for behavioral evidence of tinnitus or hyperacusis using gap and tone prepulse inhibition of the acoustic startle response. We found that sound exposure did not affect gap-prepulse inhibition. However, sound exposure led to an improvement in prepulse inhibition when the prepulse was a 7 kHz tone, showing that exposed rats had enhanced sensorimotor gating for the exposure frequency. Together, our electrophysiological and behavioral results provide evidence of hyperacusis but not tinnitus in sound-exposed animals. Our findings demonstrate that periods of prolonged noise exposure may open windows of plasticity that can also be understood as windows of vulnerability, potentially increasing the likelihood for maladaptive plasticity to take place.

SUBMITTER: Thomas ME

PROVIDER: S-EPMC6819503 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Evidence of Hyperacusis in Adult Rats Following Non-traumatic Sound Exposure.

Thomas Maryse E ME Guercio Gerson D GD Drudik Kristina M KM de Villers-Sidani Étienne É

Frontiers in systems neuroscience 20191023

Manipulations that enhance neuroplasticity may inadvertently create opportunities for maladaptation. We have previously used passive exposures to non-traumatic white noise to open windows of plasticity in the adult rat auditory cortex and induce frequency-specific functional reorganizations of the tonotopic map. However, similar reorganizations in the central auditory pathway are thought to contribute to the generation of hearing disorders such as tinnitus and hyperacusis. Here, we investigate w ...[more]

PMID: 31708754

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Project description:ObjectivesHyperacusis, defined as decreased tolerance to sound at levels that would not trouble most individuals, is frequently observed in individuals with autism spectrum disorder (ASD). Despite the functional impairment attributable to hyperacusis, little is known about its prevalence or natural history in the ASD population. The objective of this study was to conduct a systematic review and meta-analysis estimating the current and lifetime prevalence of hyperacusis in children, adolescents, and adults with ASD. By precisely estimating the burden of hyperacusis in the ASD population, the present study aims to enhance recognition of this particular symptom of ASD and highlight the need for additional research into the causes, prevention, and treatment of hyperacusis in persons on the spectrum.DesignWe searched PubMed and ProQuest to identify peer-reviewed articles published in English after January 1993. We additionally performed targeted searches of Google Scholar and the gray literature, including studies published through May 2020. Eligible studies included at least 20 individuals with diagnosed ASD of any age and reported data from which the proportion of ASD individuals with current and/or lifetime hyperacusis could be derived. To account for multiple prevalence estimates derived from the same samples, we utilized three-level Bayesian random-effects meta-analyses to estimate the current and lifetime prevalence of hyperacusis. Bayesian meta-regression was used to assess potential moderators of current hyperacusis prevalence. To reduce heterogeneity due to varying definitions of hyperacusis, we performed a sensitivity analysis on the subset of studies that ascertained hyperacusis status using the Autism Diagnostic Interview-Revised (ADI-R), a structured parent interview.ResultsA total of 7783 nonduplicate articles were screened, of which 67 were included in the review and synthesis. Hyperacusis status was ascertained in multiple ways across studies, with 60 articles employing interviews or questionnaires and seven using behavioral observations or objective measures. The mean (range) age of samples in the included studies was 7.88 years (1.00 to 34.89 years). The meta-analysis of interview/questionnaire measures (k(3) = 103, nASD = 13,093) estimated the current and lifetime prevalence of hyperacusis in ASD to be 41.42% (95% CrI, 37.23 to 45.84%) and 60.58% (50.37 to 69.76%), respectively. A sensitivity analysis restricted to prevalence estimates derived from the ADI-R (k(3) = 25, nASD = 5028) produced similar values. The estimate of current hyperacusis prevalence using objective/observational measures (k(3) = 8, nASD = 488) was 27.30% (14.92 to 46.31%). Heterogeneity in the full sample of interview/questionnaire measures was substantial but not significantly explained by any tested moderator. However, prevalence increased sharply with increasing age in studies using the ADI-R (BF10 = 93.10, R2Het = 0.692).ConclusionsIn this meta-analysis, we found a high prevalence of current and lifetime hyperacusis in individuals with ASD, with a majority of individuals on the autism spectrum experiencing hyperacusis at some point in their lives. The high prevalence of hyperacusis in individuals with ASD across the lifespan highlights the need for further research on sound tolerance in this population and the development of services and/or interventions to reduce the burden of this common symptom.

Project description:Individuals with post-traumatic stress disorder (PTSD) often use alcohol to cope with their distress. This aberrant use of alcohol often develops into alcohol use disorder (AUD) leading to high rates of PTSD-AUD co-occurrence. Individuals with comorbid PTSD-AUD have more intense alcohol cravings and increased relapse rates during withdrawal than those with AUD alone. Also, individuals with PTSD or AUD alone often show similar psychological behaviors, such as impulsivity and anhedonia. Extensive clinical studies on the behavioral effects of PTSD-AUD comorbidity, namely alcohol use, have been performed. However, these effects have not been well studied or mechanistically explored in animal models. Therefore, the present study evaluated the effects of traumatic stress comorbid with alcohol exposures on ethanol intake, impulsivity, and anhedonia in mice. Adult male C57Bl/6 mice were first exposed to either mouse single-prolonged stress (mSPS), an animal model that has been validated for characteristics akin to PTSD symptoms, or control conditions. Baseline two-bottle choice ethanol consumption and preference tests were conducted after a 7-day isolation period, as part of the mSPS exposure. Next, mice were exposed to air or chronic intermittent ethanol (CIE), a vapor-induced ethanol dependence and withdrawal model, for 4 weeks. Two-bottle choice ethanol drinking was used to measure dependence-induced ethanol consumption and preference during periods intervening CIE cycles. The novelty suppressed feeding (NSF) test was used to evaluate impulsivity and anhedonia behaviors 48 h after mSPS and/or repeated CIE exposure. Results showed that, compared to control conditions, mSPS did not affect baseline ethanol consumption and preference. However, mSPS-CIE mice increased Post-CIE ethanol consumption compared to Control-Air mice. Mice exposed to mSPS had a shorter latency to feed during the NSF, whereas CIE-exposed mice consumed less palatable food reward in their home cage after the NSF. These results demonstrate that mice exposed to both mSPS and CIE are more vulnerable to ethanol withdrawal effects, and those exposed to mSPS have increased impulsivity, while CIE exposure increases anhedonia. Future studies to examine the relationship between behavioral outcomes and the molecular mechanisms in the brain after PTSD-AUD are warranted.

Project description:Stress early in life can have a major impact on brain development, and there is increasing evidence that childhood stress confers vulnerability for later developing psychiatric disorders. In particular, during peri-adolescence, brain regions crucial for emotional regulation, such as the prefrontal cortex (PFC), amygdala (AMY) and hippocampus (HPC), are still developing and are highly sensitive to stress. Changes in myelin levels have been implicated in mental illnesses and stress effects on myelin and oligodendrocytes (OLs) are beginning to be explored as a novel and underappreciated mechanism underlying psychopathologies. Yet there is little research on the effects of acute stress on myelin during peri-adolescence, and even less work exploring sex-differences. Here, we used a rodent model to test the hypothesis that exposure to acute traumatic stress as a juvenile would induce changes in OLs and myelin content across limbic brain regions. Male and female juvenile rats underwent 3 h of restraint stress with exposure to a predator odor on postnatal day (p) 28. Acute stress induced a physiological response, increasing corticosterone release and reducing weight gain in stress-exposed animals. Brain sections containing the PFC, AMY and HPC were taken either in adolescence (p40), or in adulthood (p95) and stained for markers of OLs and myelin. We found that acute stress induced sex-specific changes in grey matter (GM) myelination and OLs in both the short- and long-term. Exposure to a single stressor as a juvenile increased GM myelin content in the AMY and HPC in p40 males, compared to the respective control group. At p40, corticosterone release during stress exposure was also positively correlated with GM myelin content in the AMY of male rats. Single exposure to juvenile stress also led to long-term effects exclusively in female rats. Compared to controls, stress-exposed females showed reduced GM myelin content in all three brain regions. Acute stress exposure decreased PFC and HPC OL density in p40 females, perhaps contributing towards this observed long-term decrease in myelin content. Overall, our findings suggest that the juvenile brain is vulnerable to exposure to a brief severe stressor. Exposure to a single short traumatic event during peri-adolescence produces long-lasting changes in GM myelin content in the adult brain of female, but not male, rats. These findings highlight myelin plasticity as a potential contributor to sex-specific sensitivity to perturbation during a critical window of development.

Dataset Information

Evidence of Hyperacusis in Adult Rats Following Non-traumatic Sound Exposure.

Publications

Evidence of Hyperacusis in Adult Rats Following Non-traumatic Sound Exposure.

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