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

Aim To study the protective effects of Presumptive endotheliumartmendependent hyperpolarizing factor(EDHF)released from the rat middle cerebral arteries(MCA),which was mediated by acetylcholine(ACh),on primarily cultured hippocampal neurons subjected to hypoxia-reoxygenation injury.Methods Primarily cultured hippocampal neurons was insulted by hypoxia-reoxygenation;EDHF was produced in rat MCA ring by 1 ?mol?L-1 ACh in the presence of NG-nitro-L-argininemethyl ester(L-NAME,a NOS inhibitor)and indomethcacin(Indo,a COX inhibitor);MTT absorbance and the LDH activity were served as the cell injury index,The level of free calcium fluorescence intensity in the cultured hippocampal neurons was monitored by laser scanning confocal microsope.Results Compared with nomal group,MTT absorbance were decreased significantly,LDH activity in the supernate culture fluid and the Ca2+ in hippocampal neurons increased significantly in model group.The conjoined use of 1 ?mol?L-1 ACh and the endothelium-intacted MCA(MCA/Endo)or ACh+MCA/Endo+L-NAME+Indo can repress both the decrease of MTT absorbance and the increases of LDH activity in the supernate culture fluid and the Ca2+ in neurons which resulted from hypoxia-reoxygenation injury;Neither 1 ?mol?L-1ACh alone nor MCA/Endo alone has the similar effects mentioned above,the conjoined use of 1 ?mol?L-1 ACh and the endothelium-denuded MCA(ACh+MCA/-Endo)also has little effect.K+ which concentration is between 25~35 ?mol?L-1 can significantly attenuate the effects afforded by the conjoined use of 1 ?mol?L-1 ACh,MCA/Endo,L-NAME and Indo,but it is not the same situation when it comes to Ba2+.Conclusions Presumptive EDHF can protect primarily cultured rat hippocamal neurons insulted by hypoxia-reoxygenation and the mechanism is partially concerned with the inhibition of calcium overload.

The interaction mechanism between rhaponticin (RT) and human serum albumin (HSA) has been studied by fluorescence spectroscopy and absorbance spectra. The mediation effect that the metal ions took part in the interaction has also been discussed in this paper. Based on different theoretical models of fluorescence quenching, the binding constant (K) and binding sites (n) of the interaction were determined and analyzed comparatively. The quenching mechanism of the binding reaction has also been discussed. The binding distance (r) and energy-transfer efficiency (E) between RT/RT-Co(II)/RT-Ni(II) and HSA were also obtained by virtue of the Förster theory of non-radiation energy transfer. The effect of RT acting on the HSA's conformation was analyzed by synchronous fluorescence spectroscopy. The result showed that the result calculated by different theoretical models is generally equivalent and RT bound HSA strongly by forming stable complex, which indicates that HSA under physiological conditions can act as a carrier for RT to be transported to exert effects. The microconformation of HSA changed significantly due to hydrophobicity change in the chemical environment of some fluorescence chromophores in the subdomain IIA and IIB of HSA. Metal ions Co(II) and Ni(II) can mediate RT-HSA interaction, making the binding of the drug to protein stronger, which indicates that Co(II) and Ni(II) can enhance rhaponticin's medical efficacy under physiological conditions.

Aim To study the protective effect of total flavones of rhododendra pharmacological preconditioning(TFR-PP)on myocardial ischemia and reperfusion injury and its mechanisms involved in myocardial inflammation in rats.Methods In model group the isolated perfused rat hearts set up by Langendorff system were subjected to 30 min ischemia followed by 40 min reperfusion. The hearts in TFR-PP groups were subjected to three cycles of 5 min perfusion with and without TFR before 30 min ischemia followed by 40 min reperfusion. In all groups the activities of lactate dehydrogenase (LDH), creatine phosphokinase (CK), and myeloperoxidase (MPO) in myocardium, the expressions of nuclear factor-kappa B (NF-?B), tumor necrosis factor-alpha(TNF-?), and intercellular adhersion molecule-1 (ICAM-1) were measured, and the myocardial pathomorphological changes were examined.Results TFR-PP(25、50、100 mg?L-1) could inhibit markedly the reductions of LDH and SOD activities in myocardium induced by ischemia and reperfusion injury.100 mg?L-1 TFR-PP also significantly improved the pathomorphological changes of injury. TFR-PP (25、50、100 mg?L-1) could inhibit the expressions of NF-?B, TNF-? and ICAM-1 to varying degrees.Conclusion TFR-PP has marked protective effect on ischemia and reperfusion injury in isolated rat heart via inhibiting the inflammation of myocardium.

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 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.

Aim To observe the neuroprotective effect of sinomenine on hippocampal neurons from injury in-duced by oxygen glucose deprivation ( OGD ) and its underlying mechanism. Methods Hippocampal neu-rons were exposed to OGD for 4 h followed by 24 h re-oxygenation ( OGD-R) . Then cell viability was detec-ted by MTT. LDH release was detected by LDH kit. Cell apoptosis was detected by Hoechst stain. The ex-pression of Bax, Bcl-2 and caspase-3 were detected by Western blot. [ Ca2+] i of hippocampal neurons was detected by calcium imaging. Acid-sensing ion chan-nels ( ASICs ) current was detected by patch clamp technique. Results SN increased cell viability and reduced LDH release. SN also inhibited neuron apop-tosis and increased ratio of Bcl-2/Bax and reduced the expression of caspase-3 . OGD-induced increase of [ Ca2+] i was inhibited by SN. Furthermore, SN inhib-ited ASIC1 a current and also inhibited OGD induced increase of ASICs current in hippocampal neurons. Conclusion SN protects hippocampal neurons against OGD-R-induced injury. The inhibitory effect of SN on ASIC1 a and calcium overload was involved in the pro-tective effect of SN.

Objective To investigate the effect of stroke unite on brain stem infarction.Methods 102 patients with brain stem infarction from Janualy 2005 to May 2009 were randomly divided into two groups:treatment group with stroke unite(n=52) and control group(n=50).Patients in treatment group were administrated stroke unite for four weeks.Cases in control group were given traditional treatment for the same time.The primary efficacy was evaluated by NIHSS(the National Institutes of Health stroke scale,NIHSS),ADL(Activities of daily living,ADL) and clinical effective.The data were analyzed by SPSS12.0 software package.The difference was significant if P

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.