| Age-related hearing impairment is one of the common problems that elder people were facing. The decreased ability of intensity tuning and narrowed dynamic range is the most common symptoms of age-related hearing impairment. Past research focused on the peripheral level, central mechanism is not yet clear, we also did not understand the relationship between morphology and function. This experiment combined the electrophysiological and histomorphology method, using the adult and aged mouse (Mus musculus, Km) as model animal, exploring the cause of the degeneration of central nucleus’ability of intensity tuning and the options of improvement, putting forward the new ways to treat the age-related hearing impairment and to protect hearing.In this experiment, we used extracellular single unit recording in the free-field sound stimulation.144 neurons were recorded, including 70 inferior colliculu (IC) neurons of aged mouse and 74 IC neurons of adult mouse. The firing duration of IC neurons in aged mouse was 4.8 ms shorter than adult mouse (p<0.01), the percent of ongoing neurons in aged mouse was 16.0% less than adult mouse, the best frequency (BF) of IC neurons in aged mouse was 5.4 kHz lower than adult mouse (p<0.001), and mainly focused on middle and high frequency IC neurons (both p<0.01). Minimum threshold (MT) of IC neurons in aged mouse was 18.7 dB SPL higher than adult mouse (p<0.001), the MT of low, middle, high frequency IC neurons were higher than adult mouse (all p<0.001). The first spike latency (FSL) of IC neurons in aged mouse was 3.9 ms longer than adult mouse (p<0.001), FSL of low and high frequency IC neurons in aged mouse was longer than adult mouse (both p<0.05); these results showed that aged mouse had a decreased acoustic signal coding ability and a more obvious hearing loss in high frequency. We thought these changes were related to the degenerated function of peripheral auditory organ and lower auditory center.In this experiment, we obtained rate-intensity functions (RIFs) of 70 IC neurons in aged mouse and 74 IC neurons in adult mouse. Non-monotonic RIFs of IC neurons in aged mouse was 5.4% less than adult mouse; dynamic range (DR) of IC neurons in aged mouse was 8.9 dB less than adult mouse (p<0.001); middle DR intensity (mDR) of IC neurons in aged mouse 15.2 dB SPL was higher than adult mouse (p<0.001); these data indicated that IC neurons of aged mouse had a narrower intensity range, and shifted to the high intensity. In high intensity, there is no significant difference in spikes (p>0.05) and FSL (p>0.05) of IC neurons between aged mouse and adult mouse. There was no influence on the ability of encoding intensity of IC neurons in aged mouse, under the condition of damaged hair cells in peripheral auditory organ along with the decreased excitatory input, high-threshold inhibitory input that aged mouse IC neurons in aged received was reduced, retaining the response ability to the high intensity in aged mouse.In this experiment, we used Nissl’s staining method to count the number of IC neurons in adult mouse and aged mouse, founding that the number of IC neurons in aged mouse was 15.2% less than adult mouse (p<0.001); using immunohistochemical staining to count the number of γ-aminobutyric acid (GABA) neurons, the results showed that GABAergic neurons in aged mouse was 23.4% less than adult mouse (p<0.001). The percent of GABAergic neurons of IC neurons in aged mouse decreased by 5.1%(p<0.05). The reduction in the number of GABAergic neurons in aged mouse may be related to the declined intensity selectivity.In addition, we also studied the duration selectivity of primary auditory cortex neurons in adult mouse, but it was not clear whether the intensity of acoustic signal will have an influence on the duration selectivity characteristics of A1 neurons in mouse. In this experiment, we used extracellular single unit recording in the free-field sound stimulation, and obtained 35 A1 neurons:duration selectivity neurons 57.1%(20/35), including short-pass 20.0%(7/35), band-pass 5.7%(2/35), band-off 8.5%(3/35), long-pass 22.9%(8/35), non-duration selectivity neurons, all-pass 42.9%(15/35). There are 62.9%(22/35) unaffected A1 neurons, including 20.0%(7/35) duration selectivity neurons and 42.9%(15/35) non-duration selectivity neurons; 37.1%(13/35) affected A1 neurons were duration selectivity neurons. BF of the affected duration selectivity A1 neurons was 6.5 kHz (p<0.05) higher than unaffected duration selectivity A1 neurons. Our results indicated that duration selectivity of most A1 neurons in mouse will be reduced along with intensity of elevated acoustic signal, duration selectivity may be attributed to increase of excitatory input and saturation inhibitory input activated by high threshold. |
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