ABSTRACT
Objective To investigate the neural activity in the central auditory pathway by using a tinnitus an-imal model .Methods Twenty -four rats were randomly divided into the control ,acute salicylate treatment ,chronic salicylate treatment ,and recovery groups .The gap prepulse inhibition of acoustic startle test was used to confirm tinnitus -like behavior .After delivery of an intravenous bolus of fluorine -18 fluorodeoxyglucose (18F -FDG ) , small animal positron emission tomography scans were performed on rats .Results Only rats in chronic salicylate -treatment group showed evidence of experiencing tinnitus .The SUV ratios of the AC were significantly greater in the acute salicylate treatment group than in the control group (P<0 .01) ,suggesting relatively increased metabolism in the two brain regions of the rats in this group .The SUV ratios of the IC and AC (P<0 .01) ,but not of the CRB (P>0 .05) were greater in the chronic salicylate treatment group than in the control groups .There was a significant difference in whole brain SUVs between the control and acute salicylate treatment groups (P<0 .01) ,the whole brain SUVs in chronic salicylate treatment group were a little higher but showed no significant difference (P>0 .05) .There was no significant difference in the SUVs between the control and recovery groups (P>0 .05) .Conclu-sion These findings indicate that long -term salicylate administration induced tinnitus in rats and may have en-hanced neural activity corresponded to the up -regulated metabolic rate in our study .Alterations to neuroplasticity of the CNS may lead to tinnitus .
ABSTRACT
OBJECTIVE To observe the changes of synaptic ultrastructures in the rat auditory center after long-term salicylate administration and to elucidate the role of neuroplasticity in some areas of the CNS and its involvement in tinnitus. METHODS The rats were divided into 4 groups: the control group, the acute treatment group, the chronic treatment group, and the recovery group. We investigated ultrastructural alterations in the synapses of inferior colliculus (IC), auditory center (AC) and cerebellum (CRB) by transmission electron microscopy. RESULTS There were more synaptic vesicles (tIC=-4. 61, tAC=-7. 00, P＜0. 01), with greater postsynaptic densities(tIC=-4. 72,P＜0. 01; tAc=-3. 15, P＜0. 05), longer synaptic active zone (tIC=-4. 89, tAC=-3. 48, P＜ 0. 01), and increased synaptic interface curvature (tIC=-2. 32, tAC=-3. 17, P＜0. 05) in the chronic treatment group, as compared with the control group. There were more synaptic vesicles but no other changes in the acute salicylate-treatment group(tIC=-10. 57, tAC=-8. 34, tCRB=-9. 18,P ＜0. 01). CONCLUSION These findings showed that long-term salicylate administration have induced synaptic ultrastructural changes in the IC and AC because of neuroplasticity. These structural changes may result in increased speed and efficacy of chemical synaptic transmission. Alterations to neuroplasticity of the auditory center pathway may lead to tinnitus.
ABSTRACT
Adult guinea pigs with normal Preyer's reflexs were used in this experiment and were divided into three groups according to the intensity of noise and exposure time. Auditory brainstem evoked response was recorded before and after exposure to noise. Clicks were presented monaurally at a rate of high (50 Hz) as well as low (10 Hz). The superior olive and inferior colliculus were observed under the electron microscope after the guinea pigs were exposured to 110dB noise for 30 min. The average shift of wave Ⅳ amplitude-intensity function curve was more than that of wave I after exposure to intensive noise. The difference value of wave Ⅴ latency from low (10 Hz) to high (50 Hz) stimulus click rate decreased and was negatively co related with the exposure time. Ⅰ-Ⅴ, Ⅲ -Ⅴ and Ⅳ-Ⅴ interpeak latencies were shorter after exposure to noise. The mitochondria and neurilemma swelling were found in the superior olive and inferior colliculus after exposure. Some mechanisms of the changes of auditory center were discussed in this paper.