Tinnitus is the most common disease in Otology, and extremely difficult for treatment in clinic, abnormal events in the cochlea (the abnormal events can result in abnormal neuronal activity in central auditory pathways that can then be finally perceived as tinnitus). Neuroplasticity events at the auditory cortex (AC) have been reported to include hyperactive of cortical neurons and an increase in neuronal synchronization. Our recent studies showed the changes markedly, in the expression of the excitatory glutamate receptor subtype NR2B in mRNA and protein levels, and also some changes in synaptic ultrastructure of neurons in auditory cortex of tinnitus animal. We propose that the mechanisms of tinnitus centralization may arise from abnormal events in the cochlea, and result in abnormal neuronal activity at multiple levels which promote abnormal propagation of neural activity in the central auditory pathway. The plastic change may be positive and adaptive as with learning or memory, or in the compensation after abnormal events in the cochlea that results in new neuronal networks that restore normal function. Alternatively, the neuroplasticity changes might be maladaptive leading perhaps to an imbalance in excitatory and inhibitory events in the brain. Indeed, tinnitus may be the consequence of such maladaptive neuroplasticity brain alterations (synaptic structure) has even gone a step further and described tinnitus as the perceptual manifestation of plastic brain changes that result in abnormal neuronal activity. The neuroplasticity changes may also make tinnitus persists, eventually leading to the existence of tinnitus cochlear-originated in the central pathway. They may also extend to non-sensory areas of the brain giving rise to the attentional and emotional aspects that often accompany the disorder. New pathophysiological insights maybe prompt the development of management approaches to directly target the neuroplasticity processes correlates of tinnitus.
Auditory Cortex ; Humans ; Neuronal Plasticity ; Tinnitus ; diagnosis ; etiology ; therapy

Objective To observe effect of olivo-cochlear feedback produced by a contralateral noise on the inhibition of electrophysiological cochleaoneural activity under sedation and anesthesia with or without maintenance of temperature to investigate the effect of sedation and anesthesia on the cochlear efferent system function. Methods The recording of electrophysiological cochleoneural activity was to implant an electrode at the round window, the ASECA (average spectrum of electrophysiological cochleaoneural activity) was obtained to FFT transform for the signal recorded. Results The results indicated that the effects of contralateral noise on ASECA were notably diminished during sedation and were almost completely suppressed during anesthesia either with or without maintenance temperature. Conclusion The present study shows that sedation and anesthesia respectively diminish and suppresse the cochlear efferent system functions.

Objective To study the change and the characteristics of distortion product otoacoustic emissions (DPOAE) of awake guinea pigs with the acute injection of sodium salicylate, and to investigate the ototoxicity of sodium salicylate to OHC. Methods With CELESTA 503 otoacoustic emission analyzer, DPOAE including DP-gram and DP-I/O function of awake guinea pigs were recorded.DPOAE were measared before and 2,4,8 h after acute injection of sodium salicylate or saline respectively. The data were analysed with SPSS 10.0.Results Acute sodium salicylate injection mainly caused the DPOAE amplitude and the I/O slope to reversibly decrease and increase respectively. The changes were largest 2 h after injection, and almost returned to normal level 8 h after injection. The differences between certain outcomes of DPOAE after and before injection were significant (P

Objective To get the thresholds of single and simultaneously multiple bone conduction auditory steady-state response(BC-ASSR) of young adults with normal hearing,and to compare the thresholds obtained with the two methods.Methods BC-ASSR to single and simultaneously multiple stimuli and PTA were examined in 28(56 ears ) young adults with normal hearing.Results At 0.5,1,2,4 kHz,the thresholds of BC-ASSR to single stimuli were 53,47,53,51 dB SPL respectively;the thresholds of BC-ASSR to simultaneously multiple stimuli were 59,54,63,61 dB SPL respectively.There were significant differences between the two at each frequency. Conclusion There are some difference between the thresholds of ASSR to single and simultaneously multiple bone conduction stimuli,especially at the higher frequencies.

Objective To investigate the influence of long-term sound conditioning on the physiology of outer hair cells.Methods Twenty healthy guinea pigs were exposed to a broadband noise for 14 days consecutively at the level 90 dB(A),8 h/day.The DP-gram and input/output(I/O)function(1~8 kHz)were measured at pre-conditioning,fourteen days conditioning,seven days post-conditioning and fourteen days post-conditioning,respectively.Results The results of DP-gram measurements demonstrated that long-term sound conditioning could enhance the DPOAE amplitudes within low frequencies(1~3 kHz,especially 5.0 dB at 2 kHz and 7.5 dB at 3 kHz,P

Objective To investigate the different expression levels of Na+-K+-2Cl-co-transporter NKCC1 mRNA in the cochlea of rats after sodium salicylate injection and to explore the mechanism underlying the change of outer hair cells,induced by different salicylate administration.Methods Twenty-four normal adult rats were randomly divided into four groups with six rats in each group. Rats in control group,did not recieve sodium salicylate injection. The other three groups were acute group,chronic group,and recovered group according to the different doses of sodium salicylate.The fluorescence quantitative PCR method was used to detect the expression levels of NKCC1 mRNA in the rat cochleas of the four groups.Results NKCC1 mRNA was expressed in all of the four groups.After sodium salicylate injection,the expressions of NKCC1 mRNA in chronic and recovered group were higher than that in control group(P

Objective To investigate the different expression levels of Na+ - K+ - 2Cl- co- transporter NKCC1 mRNA in the cochlea of rats after sodium salicylate injection and to explore the mechanism underlying the change of outer hair cells, induced by different salicylate administration. Methods Twenty-four normal adult rats were randomly divided into four groups with six rats in each group. Rats in control group,did not recieve sodium sa-licylate injection. The other three groups were acute group,chronic group,and recovered group according to the dif-ferent doses of sodium salicylate. The fluorescence quantitative PCR method was used to detect the expression levels of NKCC1 mRNA in the rat cochleas of the four groups. Results NKCC1 mRNA was expressed in all of the four groups. After sodium salicylate injection, the expressions of NKCC1 mRNA in chronic and recovered group were higher than that in control group(P<0.05). While the expression of NKCC1 mRNA in acute group was lower than that in control group(P(0. 05). Conclusion The expression of NKCC1 mRNA in the normal cochlea indicates that NKCC1 may play an important role in the maintenance of Cl- in the endolymph of the cochlea. The alteration of NKCC1 mRNA expression caused by sodium salicylate injection may lead to the change of the outer hair cell electro-motility.

AIM: To study the origin of the 1kHz peak of average spectrum electrophysiological cochleoneural activity (ASECA-1kHz),which is related to the firing of auditory neurous-a possible synchronized firing. METHODS: By using the various sound presented either ipsilaterally or contralaterally,the alterations of ASECA-1kHz were detected under the state of awakness. RESULTS: (1) Contralateral stimulation with noise bands at frequencies above 8kHz and below acoustic interaural cross-talk decreased the amplitude of ASECA-1kHz. (2) For the presentations of ipsilaterally noises,when the acoustic bandwidth was above or below 1.5kHz,then produced respectively an increase or a decrease of ASECA-1kHz. (3) Pure tones when presented contralaterally had no detectable effect,but when presented ipsilaterally pure tones with frequencies higher than 4kHz decreased the ASECA-1kHz. Moreover,the detailed time course of sound-induced variations of the 1kHz peak was measured by time averaging,the resulting response patterns were resemblance to PST histogram of the auditory nerve. CONCLUSIONS: The results suggest that the ASECA-1kHz peak in the guinea pig originates from a restricted tonotopic area corresponding to the high frequencies of 12.5-25 kHz and that it should correspond to a synchronized spontaneous firing of fibers.

AIM: To find the evidence of electrophysi ol ogic mechanisms associated with average spectrum of electrophysiological cochleo neural activity (ASECA), a measure of spontaneous auditory nerve activity altera tions. METHODS: The long-term salicylate treatment was used to establis h the available animal model of tinnitus, the ASECA was monitored, and the effec ts of various presented ipsilateral acoustic were investigated. RESULTS: (1) In the first treatment, ASECA decreased acutely dur ing several hours after salicylate administration. After several days (1 week an d 2 weeks) this decrease was reduced. (2) Over weeks of salicylate administratio n, the level of ASECA increased progressively, but at the end of treatment, acou stic tuning of ASECA showed a partially decreased sensitivity. (3) In control an imals, delivery of an ipsilateral noise reproduced the increase in the level of ASECA that was similar to the result observed in long-term salicylate-treated an imals. The noise (the white noise was 55-60 dB SPL) was of moderate level and it slightly elevated CAP thresholds at higher frequencies. CONCLUSION: In the long-term salicylate-treated animals, the ASE CA-1 kHz increased reflects strongly increased synchronized activity in the audi tory nerve.

Objective To evaluate the role of δ receptor in reduction of hypoxia-reoxygenation (H/R) injury to cardiomyocytes by morphine preconditioning in rats with chronic heart failure.Methods Adult male Sprauge-Dawley rats weighing 220-250 g were used in the study.Chronic heart failure was induced by injection of adriamycin 2 mg/kg via the tail vein once a week for 6 weeks.Their hearts were removed 2 weeks after the last injection and the cardiomyocytes were isolated and cultured.The cells were randomly divided into 5 groups ( n =8 each):control group (group C); H/R group; morphine preconditioning group (group MPC); morphine preconditioning + naloxone (opioid receptor antagonist ) group (group MPC + Naloxone) ; morphine preconditioning + naltrindole ( δ receptor antagonist) group ( MPC + Naltrindole group).The cells were cultured in normal culture atmosphere in group C and were exposed in hypoxic air for 3 h followed by 1 h reoxygenation in the other groups.Morphine preconditioning was performed immediately before hypoxia in group MPC.Naloxone and naltrindole were added before morphine preconditioning in groups MPC + Naloxone and MPC + Natrindole respectively.At 1 h of reoxygenation,the cell viability ( by MTT assay),activities of lactate dehydrogenase ( LDH ) and creatine kinase (CK),and cell apoptosis were detected.The apoptotic rate was calculated.Results The cell viability was significantly lower,and the activities of LDH and CK and apoptotic rate were significantly higher in groups H/R,MPC + Naloxone and MPC + Natrindole than in group C (P ＜ 0.05).The cell viability was significantly higher,and the activities of LDH and CK and apoptotic rate were significantly lower in group MPC than in group H/R ( P ＜ 0.05).Conclusion Morphine preconditioning reduces H/R injury to cardiomyocytes through activating δ receptor in rats with chronic heart failure.