Noise And Salicylate Induce The Electrical Activity Change In Inferior Colliculus And Cortex

IntroductionTinnitus is the subjective sound sensation without corresponding external sound source orelectrical stimulation. The incidence of tinnitus is about3%-30%, about l%-3%of the everydaylife and work are affected by tinnitus. The causes of hearing loss (noise exposure, aging, drugs,trauma) are likely to induce tinnitus. Exclusion of tinnitus caused by organic disease, most oftinnitus are subjective. Due to the limit objective evaluation method of the neurogenic tinnitus,the diagnosis of localization of tinnitus is hard, it is a difficult problem for clinical treatment.The mechanism of tinnitus is not clear. Generally, the inhibition of central auditory system(CAS) decreases, causing the electrical activity change of the CAS change is tinnitusneurophysiologic basis. Neural electrical activity change of the CAS may be due to cochleardamage, it is regarded that the cochlear damage can down regulate the inhibition of some areascentral auditory system (CAS) which include auditory cortex (AC), inferior cochlear(IC) andcochlear nucleus (CN).The study on tinnitus mechanism should depend on reliable tinnitusanimal models, behavioral or electrophysiological methods, combined with the characteristics oftinnitus clinic.In this paper, we establish the animal model depending on noise exposure and high doses ofsodium salicylate (SS), the use of the electrophysiological methods to record, analyze andquantify, classify and assess changes in IC and AC.Method and resultThe first part, we use C57mice as noise exposure animal models. We use16channelmicroelectrode to get the response of IC neurons before and after the noise exposure. Thedischarge activity results include Frequency Response Area (FRA) and Rate Level Function(RLF). FRA results indicate the Characteristic Frequency (CF) of some of the IC neurons shiftfrom the high frequency area to the low frequency area after the noise exposure, the minimal threshold (MT) of some neurons is higher after the noise exposure. The BF and MT of some ofthe neurons change significantly after the noise exposure, however, BF and MT of some of theneurons do not change obviously. The RLF results show the spiking of the firing rate of eachneuron, only some of low frequency neurons show the higher firing rate after the noise exposure,however, higher frequency neurons show the lower firing rate of higher after the noise exposure.Compare the Q10value of the neurons before and after the noise exposure, it is indicated thatthe shape of the tuning curve became wider after the noise exposure, and the spontaneousactivity of each recorded neuron seems smaller than before.The second part (1) We use Sprague Dawley(SD) rats as the animal models, the16channel microelectrode is used to record the electrical activity change of AC before and afterhigh doses of SS injection. The SS can induce AC response enhancement after the intraperitonealinjection in3hours.(2) We use SD rats and microelectrode is used to record, we study on theeffect of GABA analogue and potassium channel openers. We test the spiking of the firing rateof GABAB analogue group, GABA analogue+SS group, potassium channel opener group,potassium channel opener+SS group. After the drugs injection5minutes, we injected salicylate.The response of the firing rate of GABA analogue+SS group and GABA analogue+SS groupare increased less than that in salicylate injection group. It is indicated that GABA analogue andpotassium channel opener partially suppressed SS-induced hyperactivity in AC.Conclusion(1) Noise exposure may induce damage of the side-band inhibition in the IC, theseinhibition areas in lower frequency neurons than CF of IC. CF shifts and tuning curve wider ismainly found in higher frequency neurons than noise exposure frequency. The spontaneousactivity of IC neurons is decreased at once after the noise exposure, which is different from thespontaneous activity change after a period of noise exposure. The electrical activity changeabove indicates that cochlear receives afferent signals less after noise exposure, which affect theauditory pathway, The IC plasticity change may be the cause of the tinnitus, and explains thefrequency of the noise-induced tinnitus frequency range is related to the frequency of the noiseexposure, that is, the frequency of tinnitus is often lower than that of noise exposure.(2) High doses of SS can induce the firing rate increasing, GABA analogues andpotassium channel openers can reduce the firing rate of the AC, these two drugs on affect the electrophysiological function of high doses of SS on the auditory cortex. GABA analogues andpotassium channel openers might inhibit tinnitus.