Prestin gene expression in the rat cochlea following intense noise exposure

Abstract Background This study aimed to investigate the changes in the expression of hippocampal genes upon acute noise exposure. Methods Three-week-old Sprague–Dawley rats were assigned to control (n = 15) and noise (n = 15) groups. White noise (2–20 kHz, 115 dB sound pressure level [SPL]) was delivered for 4 h per day for 3 days to the noise group. All rats were sacrificed on the last day of noise exposure, and gene expression in the hippocampus was analyzed using a microarray. Pathway analyses were conducted for genes that showed differential expression ≥ 1.5-fold and P ≤ 0.05 compared to the control group. The genes included in the putative pathways were measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Results Thirty-eight upregulated genes and 81 downregulated genes were identified. The pathway analyses revealed that upregulated genes were involved in the cellular responses to external stimuli and immune system pathways. qRT-PCR confirmed the upregulation of the involved genes. The downregulated genes were involved in neuronal systems and synapse-related pathways, and qRT-PCR confirmed the downregulation of the involved genes. Conclusions Acute noise exposure upregulated the expression of immune-related genes and downregulated the expression of neurotransmission-related genes in the hippocampus.

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Changes in endocochlear potential during anoxia after intense noise exposure

Hearing Research ◽

10.1016/0378-5955(90)90076-2 ◽

1990 ◽

Vol 44 (2-3) ◽

pp. 143-149 ◽

Cited By ~ 12

Author(s):

Jian Wang ◽

Wei-jia Dong ◽

Ji-sheng Chen

Keyword(s):

Noise Exposure ◽

Endocochlear Potential ◽

Intense Noise

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Intermittent Exposure to Noise: Effects on Hearing

Annals of Otology Rhinology & Laryngology ◽

10.1177/000348948309200618 ◽

1983 ◽

Vol 92 (6) ◽

pp. 623-628 ◽

Cited By ~ 9

Author(s):

Joseph Sataloff ◽

Robert T. Sataloff ◽

Raymond A. Yerg ◽

Hyman Menduke ◽

Robert P. Gore

Keyword(s):

Hearing Loss ◽

Noise Exposure ◽

Continuous Exposure ◽

Hearing Results ◽

Noise Effects ◽

High Frequencies ◽

Severe Loss ◽

Intermittent Exposure ◽

Intense Noise ◽

Continuous Noise

Most studies of the effects of noise upon hearing have dealt with continuous noise exposure. Previous reports on intermittent exposure to noise concluded that it causes less damage to hearing than does continuous exposure to noise of the same intensity. In this investigation, 12,000 workers were screened to find 295 subjects who met the strict criteria of the study. Most of the subjects were exposed to jackhammer noise at peak levels of 118 dBA. Intermittent exposure to intense noise results in very severe loss in high frequencies but relatively little or no hearing loss in the lower frequencies even after many years of exposure. This differs substantially from the effects of continuous exposure to noise of the same intensity. It remains to be determined whether this pattern of hearing results from intermittent exposure to all sorts of noise or only from the kinds of sources investigated in this study.

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Noise-induced hyperactivity in the inferior colliculus: its relationship with hyperactivity in the dorsal cochlear nucleus

Journal of Neurophysiology ◽

10.1152/jn.00833.2011 ◽

2012 ◽

Vol 108 (4) ◽

pp. 976-988 ◽

Cited By ~ 41

Author(s):

N. F. Manzoor ◽

F. G. Licari ◽

M. Klapchar ◽

R. L. Elkin ◽

Y. Gao ◽

...

Keyword(s):

Spontaneous Activity ◽

Inferior Colliculus ◽

Cochlear Nucleus ◽

Time Course ◽

Noise Exposure ◽

Dorsal Cochlear Nucleus ◽

Control Group ◽

Before And After ◽

Intense Noise ◽

And Control

Intense noise exposure causes hyperactivity to develop in the mammalian dorsal cochlear nucleus (DCN) and inferior colliculus (IC). It has not yet been established whether the IC hyperactivity is driven by hyperactivity from extrinsic sources that include the DCN or instead is maintained independently of this input. We have investigated the extent to which IC hyperactivity is dependent on input from the contralateral DCN by comparing recordings of spontaneous activity in the IC of noise-exposed and control hamsters before and after ablation of the contralateral DCN. One group of animals was binaurally exposed to intense sound (10 kHz, 115 dB SPL, 4 h), whereas the control group was not. Both groups were studied electrophysiologically 2–3 wk later by first mapping spontaneous activity along the tonotopic axis of the IC to confirm induction of hyperactivity. Spontaneous activity was then recorded at a hyperactive IC locus over two 30-min periods, one with DCNs intact and the other after ablation of the contralateral DCN. In a subset of animals, activity was again mapped along the tonotopic axis after the time course of the activity was recorded before and after DCN ablation. Following recordings, the brains were fixed, and histological evaluations were performed to assess the extent of DCN ablation. Ablation of the DCN resulted in major reductions of IC hyperactivity. Levels of postablation activity in exposed animals were similar to the levels of activity in the IC of control animals, indicating an almost complete loss of hyperactivity in exposed animals. The results suggest that hyperactivity in the IC is dependent on support from extrinsic sources that include and may even begin with the DCN. This finding does not rule out longer term compensatory or homeostatic adjustments that might restore hyperactivity in the IC over time.

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