Acute Noise Exposure Is Associated With Intrinsic Apoptosis in Murine Central Auditory Pathway

Abstract

Noise that is capable of inducing the hearing loss (NIHL) has a strong impact on the inner ear structures and causes early and most obvious pathophysiological changes in the auditory periphery. Several studies indicated that intrinsic apoptotic cell death mechanisms are the key factors inducing cellular degeneration immediately after noise exposure and are maintained for days or even weeks. In addition, studies demonstrated several changes in the central auditory system following noise exposure, consistent with early apoptosis-related pathologies. To clarify the underlying mechanisms, the present study focused on the noise-induced gene and protein expression of the pro-apoptotic protease activating factor-1 (APAF1) and the anti-apoptotic B-cell lymphoma 2 related protein a1a (BCL2A1A) in the cochlear nucleus (CN), inferior colliculus (IC) and auditory cortex (AC) of the murine central auditory pathway. The expression of Bcl2a1a mRNA was upregulated immediately after trauma in all tissues investigated, whereas the protein levels were significantly reduced at least in the auditory brainstem. Conversely, acute noise has decreased the expression of Apaf1 gene along the auditory pathway. The changes in APAF1 protein level were not statistically significant. It is tempting to speculate that the acoustic overstimulation leads to mitochondrial dysfunction and induction of apoptosis by regulation of proapoptotic and antiapoptotic proteins. The inverse expression pattern on the mRNA level of both genes might reflect a protective response to decrease cellular damage. Our results indicate the immediate presence of intrinsic apoptosis following noise trauma. This, in turn, may significantly contribute to the development of central structural deficits. Auditory pathway-specific inhibition of intrinsic apoptosis could be a therapeutic approach for the treatment of acute (noise-induced) hearing loss to prevent irreversible neuronal injury in auditory brain structures and to avoid profound deficits in complex auditory processing.

Acid sphingomyelinase mediates the noise‐induced liver disorder in mice

“…Next, we found that the noise caused significant apoptosis of hepatocytes which was related to mobilization of intrinsic pathway, indicating the mitochondrial associated cell loss might be one of the prominent features of noise associated damage as that was also present in periphery and central auditory pathway of mice suffering from noise trauma . The imbalance between oxidation and anti‐oxidation in our work might underlie the onset of NILD, given the oxidative stress facilitating apoptosis or lipid storage of hepatocytes .…”

“…28 Next, we found that the noise caused significant apoptosis of hepatocytes which was related to mobilization of intrinsic pathway, 29,30 indicating the mitochondrial associated cell loss might be one of the prominent features of noise associated damage as that was also present in periphery and central auditory pathway of mice suffering from noise trauma. 31 The imbalance between oxidation and anti-oxidation in our work might underlie the onset of NILD, given the oxidative stress facilitating apoptosis or lipid storage of hepatocytes. 20,22,32 We did not notice any significant response of NAD(P)H oxidase to noise stimulation, which was different from previous reports in which the enzyme played a key role in noise-induced cochlea injury, 33 suggesting that the oxidative adjustment after noise exposure is organ-or tissue-specific.…”

Persistent self‐reported ear and hearing problems among World Trade Center‐exposed firefighters and emergency medical service workers, 2001‐2017—A longitudinal cohort analysis

“…We grouped auditory issues into separate categories of discomfort within the physical ear and hearing itself. Our outcome of ear symptoms which included pain, ringing, and congestion, captured noise‐induced hearing loss caused by extremely loud bursts of sound that strongly impact inner ear structures by damaging sensory tissue and possibly causing tinnitus . Although symptoms may subside, our measure of hearing problems which included decreased hearing, hearing aid use (or recommended use) and difficulty hearing, describes the progressive degeneration of sensory tissue that can occur over time …”

Dynamic Changes in Synaptic Plasticity Genes in Ipsilateral and Contralateral Inferior Colliculus Following Unilateral Noise-induced Hearing Loss

“…Cell loss in the IC and other central auditory structures could be mediated in part by upregulation and downregulation of pro-apoptotic and anti-apoptotic genes and proteins in studies of acute and permanent noise-induced hearing loss (Groschel et al, 2018).…”