Senescence-accelerated mouse prone 8 (SAMP8) as a model of age-related hearing loss

Marie, Aurore; Larroze-Chicot, Philippe; Cosnier-Pucheu, Sylvie; González-González, Sergio

doi:10.1016/j.neulet.2017.07.037

Cited by 11 publications

(15 citation statements)

References 20 publications

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“…We observed that DPOAE amplitudes were similar at baseline (30 days of age) in NAC and vehicle treated groups ( Fig. 3A ) and the DPOAE amplitude of SAMP8 mice progressively decreased in vehicle group as we previously demonstrated [ 16 ]. However, the DPOAE amplitude of NAC treated mice were small but significantly higher at 16 kHz at 60 days of age ( Fig.…”

Section: Resultssupporting

confidence: 82%

“…ABRs are electric potentials recorded from scalp electrodes, and the first ABR wave represents the summed activity of the auditory nerve fibers contacting the IHCs. Using ABR technique, we previously demonstrated that SAMP8 strain presented a progressive ABR threshold increase from 45 days of age due to the accelerated degeneration of auditory system reaching a plateau at 148 days [ 16 ]. Here we observed that the ABR threshold values of NAC and vehicle groups were similar at baseline (30 days) ( Fig.…”

Section: Resultsmentioning

confidence: 99%

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N-acetylcysteine Treatment Reduces Age-related Hearing Loss and Memory Impairment in the Senescence-Accelerated Prone 8 (SAMP8) Mouse Model

Marie¹,

Meunier²,

Brun³

et al. 2018

Aging and disease

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Age-related hearing loss (ARHL) is the most common sensory disorder in the elderly population. SAMP8 mouse model presents accelerated senescence and has been identified as a model of gerontological research. SAMP8 displays a progressive age-related decline in brain function associated with a progressive hearing loss mimicking human aging memory deficits and ARHL. The molecular mechanisms associated with SAMP8 senescence process involve oxidative stress leading to chronic inflammation and apoptosis. Here, we studied the effect of N-acetylcysteine (NAC), an antioxidant, on SAMP8 hearing loss and memory to determine the potential interest of this model in the study of new antioxidant therapies. We observed a strong decrease of auditory brainstem response thresholds from 45 to 75 days of age and an increase of distortion product amplitudes from 60 to 75 days in NAC treated group compared to vehicle. Moreover, NAC treated group presented also an increase of memory performance at 60 and 105 days of age. These results confirm that NAC delays the senescence process by slowing the age-related hearing loss, protecting the cochlear hair cells and improving memory, suggesting that antioxidants could be a pharmacological target for age-related hearing and memory loss.

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Section: Resultssupporting

confidence: 82%

Section: Resultsmentioning

confidence: 99%

N-acetylcysteine Treatment Reduces Age-related Hearing Loss and Memory Impairment in the Senescence-Accelerated Prone 8 (SAMP8) Mouse Model

Marie¹,

Meunier²,

Brun³

et al. 2018

Aging and disease

Self Cite

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“…SAMP8 mice have been identified as a suitable model to study age-dependent disorders including senile amyloidosis, osteoporosis, cataracts, and brain atrophies ( Akiguchi et al, 2017 ; Karuppagounder et al, 2017 ; Folch et al, 2018 ; Grinan-Ferre et al, 2018 ). Furthermore, the SAMP8 strain has previously shown to exhibit an early age-dependent hearing loss ( Marie et al, 2017 ) associated with sensory, neural, and strial degeneration, which were primarily linked to oxidative stress ( Menardo et al, 2012 ; Fujimoto and Yamasoba, 2014 ; Benkafadar et al, 2019 ). The premature SAMP8 senescence causing early presbycusis was linked to altered levels of antioxidant enzymes and decreased activity of complexes I, II, and IV, which in turn lead to chronic inflammation and triggering of apoptotic cell death pathways ( Menardo et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Auditory Threshold Variability in the SAMP8 Mouse Model of Age-Related Hearing Loss: Functional Loss and Phenotypic Change Precede Outer Hair Cell Loss

Pinheiro

Adel

Knipper

et al. 2021

Front. Aging Neurosci.

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Age-related hearing loss (ARHL) is the most common sensory deficit in aging society, which is accompanied by increased speech discrimination difficulties in noisy environments, social isolation, and cognitive decline. The audiometric degree of ARHL is largely correlated with sensory hair cell loss in addition to age-related factors not captured by histopathological analysis of the human cochlea. Previous studies have identified the senescence-accelerated mouse prone strain 8 (SAMP8) as a model for studying ARHL and age-related modifications of the cochlear redox environment. However, the SAMP8 population exhibits a large variability in auditory function decline over age, whose underlying cause remains unknown. In this study, we analyzed auditory function of SAMP8 mice by measuring auditory brainstem response (ABR) thresholds at the age of 6 weeks (juvenile), 12 weeks (young adult), and 24 weeks (adult). Consistent with previous studies, SAMP8 mice exhibit an early progressive, age-related decline of hearing acuity. However, a spatiotemporal cytohistological analysis showed that the significant increase in threshold variability was not concurrently reflected in outer hair cell (OHC) loss observed in the lower and upper quartiles of the ABR threshold distributions over age. This functional loss was found to precede OHC loss suggesting that age-related phenotypic changes may be contributing factors not represented in cytohistological analysis. The expression of potassium channels KCNQ4 (KV7.4), which mediates the current IK,n crucial for the maintenance of OHC membrane potential, and KCNQ1 (KV7.1), which is an essential component in potassium circulation and secretion into the endolymph generating the endocochlear potential, showed differences between these quartiles and age groups. This suggests that phenotypic changes in OHCs or the stria vascularis due to variable oxidative deficiencies in individual mice may be predictors of the observed threshold variability in SAMP8 mice and their progressive ARHL. In future studies, further phenotypic predictors affected by accumulated metabolic challenges over age need to be investigated as potentially underlying causes of ARHL preceding irreversible OHC loss in the SAMP8 mouse model.

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“…As shown in Table 2, BWs of the SAMP8 groups were significantly lower than that of the ICR group. Marie et al reported that SAMP8 mice showed lower BWs, whereas CBA mice (normal mice from which the SAMP8 strain originated) retained stable BWs at the same age [25]. These BW changes can be explained by the decrease in muscle mass due to the advanced stage of the senescence process, as previously described by Guo et al [26].…”

Section: Csse and Appearance Changes Of Senescencementioning

confidence: 76%

Effects of Coriandrum sativum Seed Extract on Aging-Induced Memory Impairment in Samp8 Mice

et al. 2020

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The purpose of this study was to investigate whether or not Coriandrum sativum seed extract (CSSE) can ameliorate memory impairment in senescence-accelerated mouse-prone 8 (SAMP8) mice. Sixteen 10-week-old male SAMP8 mice were divided into two groups, which were orally administrated water (SAMP8(−)) or CSSE (200 mg/kg/day; SAMP8(+)). Eight 10-week-old male Institute of Cancer Research (ICR) mice were used as a normal control group and were also orally administrated water. The mean escape time in the Barnes maze test of SAMP8(−) mice was significantly longer than that of ICR mice. However, SAMP8(+) mice showed a shorter mean escape time compared to that of SAMP8(−) mice. Neurofilament messenger (m)RNA levels significantly decreased in the frontal lobe of SAMP8(−) mice when compared with ICR mice, but significantly increased in SAMP8(+) mice relative to SAMP8(−) mice. In addition, mRNA levels of inducible nitric oxide synthase (iNOS) and neuronal (n)NOS significantly increased in the frontal lobe of SAMP8(−) mice, but only the mRNA level of nNOS significantly decreased in SAMP8(+) mice. These results indicated that continuous oral administration of CSSE for 12 weeks could ameliorate aging-induced memory declines in the senescence-accelerated SAMP8 mouse model.

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Senescence-accelerated mouse prone 8 (SAMP8) as a model of age-related hearing loss

Cited by 11 publications

References 20 publications

N-acetylcysteine Treatment Reduces Age-related Hearing Loss and Memory Impairment in the Senescence-Accelerated Prone 8 (SAMP8) Mouse Model

N-acetylcysteine Treatment Reduces Age-related Hearing Loss and Memory Impairment in the Senescence-Accelerated Prone 8 (SAMP8) Mouse Model

Auditory Threshold Variability in the SAMP8 Mouse Model of Age-Related Hearing Loss: Functional Loss and Phenotypic Change Precede Outer Hair Cell Loss

Effects of Coriandrum sativum Seed Extract on Aging-Induced Memory Impairment in Samp8 Mice

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