title: Long-term changes of response in the inferior colliculus of senescence accelerated mice after early sound exposure.
abstract: Early sound exposure could alter auditory sensitivity in young animals. For example, the distribution of frequency tuning at the midbrain inferior colliculus (IC) is altered following early exposure to a tone at a moderate intensity level. Whether such neonatal change is still present in the old animals remains unknown. We studied the long-term effects of early sound exposure using a mutant strain of mice expressing accelerated senescence (SAM). Experimental animals were first exposed to a 9-kHz tone (53 dB sound pressure level (SPL)) for 30 days (10 h/day) after birth. Control animals received no tones. At the age of 15 months, responses of single IC units to sounds were studied electrophysiologically under urethane anesthesia. In the control group, we found an overall reduction in sensitivity to tones particularly at high frequencies, in comparison with normal non-senescent mice. Moreover, neurons exhibited increased spontaneous activities. These signs are consistent with accelerated senescence. Early sound exposure produced two effects in the experimental group. Firstly, IC units showed an apparent 'clustering' of best frequencies towards the frequency of the exposing tone (i.e., 9 kHz). Secondly, there was a further loss in sensitivity to tones particularly at high frequencies. Results suggest that early sound exposure has produced a long-lasting effect on frequency tuning of IC neurons. Acoustic overstimulation early in life may also accelerate the senescence of neurons or structures in the auditory system.
authors: Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
authors: T W
authors: TW
authors: Chiu
authors: Paul W F
authors: PW
authors: Poon
authors: W Y
authors: WY
authors: Chan
authors: David T W
authors: DT
authors: Yew
mesh_terms: D000161:Acoustic Stimulation / Q000009:adverse effects; D000200:Action Potentials / Q000502:physiology; D019588:Aging, Premature / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D001306:Auditory Pathways / Q000254:growth & development / Q000473:pathology / Q000503:physiopathology; D001307:Auditory Perception / Q000502:physiology; D001309:Auditory Threshold / Q000502:physiology; D016922:Cellular Senescence / Q000502:physiology*; D007245:Inferior Colliculi / Q000254:growth & development* / Q000473:pathology / Q000503:physiopathology; D051379:Mice; D008807:Mice, Inbred BALB C; D008817:Mice, Mutant Strains; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000473:pathology / Q000502:physiology; D013016:Sound / Q000009:adverse effects*; D013995:Time