MicroRNA-222 alleviates radiation-induced apoptosis by targeting BCL2L11 in cochlea hair cells.

Radiation-induced hair cell injury is detrimental for human health but the underlying mechanism is not clear. MicroRNAs (miRNAs) have critical roles in various types of cellular biological processes. The present study investigated the role of miR-222 in the regulation of ionizing radiation (IR)-induced cell injury in auditory cells and its underlying mechanism. Real-time PCR was performed to identify the expression profile of miR-222 in the cochlea hair cell line HEI-OC1 after IR exposure. miRNA mimics or inhibitor-mediated up- or down-regulation of indicated miRNA was applied to characterize the biological effects of miR-222 using MTT, apoptosis and DNA damage assay. Bioinformatics analyses and luciferase reporter assays were applied to identify an miRNA target gene. Our study confirmed that IR treatment significantly suppressed miR-222 levels in a dose-dependent manner. Up-regulation of miR-222 enhances cell viability and alleviated IR-induced apoptosis and DNA damage in HEI-OC1 cells. In addition, BCL-2-like protein 11 (BCL2L11) was validated as a direct target of miR-222. Overexpression of BCL2L11 abolished the protective effects of miR-222 in IR-treated HEI-OC1 cells. Moreover, miR-222 alleviated IR-induced apoptosis and DNA damage by directly targeting BCL2L11. The present study demonstrates that miR-222 exhibits protective effects against irradiation-induced cell injury by directly targeting BCL2L11 in cochlear cells.

The awesome power of optogenetics in hearing research.

The use of light as a tool to manipulate cellular processes or optogenetics has developed rapidly in various biological fields over the past decade. Through the addition of photosensitive proteins, light can be used to control intracellular mechanisms, map neuronal pathways, and alter variables that would be difficult to control using other mechanisms. Photons of a specific wavelength affect these light sensitive targets for in vitro or in vivo experiments. Optogenetics is beneficial because it gives the investigator spatial and temporal control over experimental variables. Precise control is achieved by sequential activation of different ion channels and the ability to non-invasively control membrane potential. In this review, we will discuss the recent use of optogenetics in biological fields to understand the role of different cell types in hearing and creating a new cochlear implant, as well as future uses such as light controlled drug delivery and gene expression.

Ionizing Radiation Blocks Hair Cell Regeneration in Zebrafish Lateral Line Neuromasts by Preventing Wnt Signaling.

Loss of hair cells occurs after radiotherapy, which is a major treatment modality for head and neck cancers. In the lateral line neuromasts of zebrafish, hair cells regenerate rapidly from supporting cells after damage from ototoxins. To investigate hair cell regeneration after radiation damage, zebrafish larvae were exposed to radiation, and hair cells were counted and cell proliferation was detected in neuromasts. After irradiation exposure, cell proliferation was inhibited in neuromasts and the number of supporting cells remained stable. There was a gradual loss of hair cells in lateral line neuromasts, which was not followed by regeneration. An activator of Wnt signaling (1-azakenpaullone) promoted robust regeneration of hair cells in irradiated neuromasts. By the quantitative real-time PCR and immunofluorescence, dkk2, an inhibitory Wnt ligand, was identified upregulated in irradiated neuromasts. Accelerating the death process of irradiated hair cells by treatment with neomycin also restored the regenerative capacity of neuromasts. However, a proportion of the new hair cells died within several days after forced regeneration and baseline activity of proliferation in supporting cells remained unimproved. In conclusion, these findings suggested that radiation suppressed hair cell regeneration in zebrafish lateral line neuromasts through inhibition of Wnt signaling in supporting cells possibly by secreting anti-proliferation factors like dkk2. Maintaining a healthy supporting cell pool is vital for regeneration of hair cells.

Pre-conditioning with near infrared photobiomodulation reduces inflammatory cytokines and markers of oxidative stress in cochlear hair cells.

Hearing loss is a serious occupational health problem worldwide. Noise, aminoglycoside antibiotics and chemotherapeutic drugs induce hearing loss through changes in metabolic functions resulting in sensory cell death in the cochlea. Metabolic sequelae from noise exposure increase production of nitric oxide (NO) and Reactive Oxygen Species (ROS) contributing to higher levels of oxidative stress beyond the physiologic threshold levels of intracellular repair. Photobiomodulation (PBM) therapy is a light treatment involving endogenous chromophores commonly used to reduce inflammation and promote tissue repair. Near infrared light (NIR) from Light Emitting Diodes (LED) at 810 nm wavelength were used as a biochemical modulator of cytokine response in cultured HEI-OC1 auditory cells placed under oxidative stress. Results reported here show that NIR PBM at 810 nm, 30 mW/cm2 , 100 seconds, 1.0 J, 3 J/cm2 altered mitochondrial metabolism and oxidative stress response for up to 24 hours post treatment. We report a decrease of inflammatory cytokines and stress levels resulting from NIR applied to HEI-OC1 auditory cells before treatment with gentamicin or lipopolysaccharide. These results show that cells pretreated with NIR exhibit reduction of proinflammatory markers that correlate with inhibition of mitochondrial superoxide, ROS and NO in response to continuous oxidative stress challenges. Non-invasive biomolecular down regulation of proinflammatory intracellular metabolic pathways and suppression of oxidative stress via NIR may have the potential to develop novel therapeutic approaches to address noise exposure and ototoxic compounds associated with hearing loss.

Radioprotective Effect of Aminothiol PrC-210 on Irradiated Inner Ear of Guinea Pig.

Radiotherapy of individuals suffering with head & neck or brain tumors subserve the risk of sensorineural hearing loss. Here, we evaluated the protective effect of Aminothiol PrC-210 (3-(methyl-amino)-2-((methylamino)methyl)propane-1-thiol) on the irradiated inner ear of guinea pigs. An intra-peritoneal or intra-tympanic dose of PrC-210 was administered prior to receiving a dose of gamma radiation (3000 cGy) to each ear. Auditory Brainstem Responses (ABRs) were recorded one week and two weeks after the radiation and compared with the sham animal group. ABR thresholds of guinea pigs that received an intra-peritoneal dose of PrC-210 were significantly better compared to the non-treated, control animals at one week post-radiation. Morphologic analysis of the inner ear revealed significant inflammation and degeneration of the spiral ganglion in the irradiated animals not treated with PrC-210. In contrast, when treated with PrC-210 the radiation effect and injury to the spiral ganglion was significantly alleviated. PrC-210 had no apparent cytotoxic effect in vivo and did not affect the morphology or count of cochlear hair cells. These findings suggest that aminothiol PrC-210 attenuated radiation-induced cochlea damage for at least one week and protected hearing.

Dexamethasone Protects Against Radiation-induced Loss of Auditory Hair Cells In Vitro.

HYPOTHESIS: Dexamethasone (DXM) protects against radiation-induced loss of auditory hair cells (HCs) in rat organ of Corti (OC) explants by reducing levels of oxidative stress and apoptosis. BACKGROUND: Radiation-induced sensorineural hearing loss (HL) is progressive, dose-dependent, and irreversible. Currently, there are no preventative therapeutic modalities for radiation-induced HL. DXM is a synthetic steroid that can potentially target many of the pathways involved in radiation-induced ototoxicity. METHODS: Whole OC explants were dissected from 3-day-old rat cochleae exposed to specific dosages of single-fraction radiation (0, 2, 5, 10, or 20 Gy), were either untreated or treated with DXM (75, 150, 300 µg/mL), and then cultured for 48 or 96 hours. Confocal microscopy for oxidative stress (CellRox, 48 h) and apoptosis (TUNEL assay, 96 h) and fluorescent microscopy for viable HC counts (fluorescein isothiocyanate-phalloidin, 96 h) were performed. Analysis of variance and Tukey post hoc testing were used for statistical analysis. RESULTS: Radiation exposure initiated dose-dependent losses of inner and outer HCs, predominantly in the basal turns of the OC explants. DXM protected against radiation-induced HC losses in a dose-dependent manner. DXM significantly reduced levels of oxidative stress and apoptosis in radiation-injured OC explants (p < 0.001). CONCLUSIONS: Radiation-initiated HC losses were dose-dependent in OC explants. DXM treatment protected explant HCs against radiation-initiated losses by decreasing the levels of oxidative stress and apoptosis. DXM may potentially be a therapeutic modality for preventing radiation-induced HL; further in vivo studies are necessary.

Cellular signaling protective against noise-induced hearing loss ­ A role for novel intrinsic cochlear signaling involving corticotropin-releasing factor?

Hearing loss afflicts approximately 15% of the world's population, and crosses all socioeconomic boundaries. While great strides have been made in understanding the genetic components of syndromic and non-syndromic hearing loss, understanding of the mechanisms underlying noise-induced hearing loss (NIHL) have come much more slowly. NIHL is not simply a mechanism by which older individuals loose their hearing. Significantly, the incidence of NIHL is increasing, and is now involving ever younger populations. This may predict future increased occurrences of hearing loss. Current research has shown that even short-term exposures to loud sounds generating what was previously considered temporary hearing loss, actually produces an almost immediate and permanent loss of specific populations of auditory nerve fibers. Additionally, recurrent exposures to intense sound may hasten age-related hearing loss. While NIHL is a significant medical concern, to date, few compounds have delivered significant protection, arguing that new targets need to be identified. In this commentary, we will explore cellular signaling processes taking place in the cochlea believed to be involved in protection against hearing loss, and highlight new data suggestive of novel signaling not previously recognized as occurring in the cochlea, that is perhaps protective of hearing. This includes a recently described local hypothalamic-pituitary-adrenal axis (HPA)-like signaling system fully contained in the cochlea. This system may represent a local cellular stress-response system based on stress hormone release similar to the systemic HPA axis. Its discovery may hold hope for new drug therapies that can be delivered directly to the cochlea, circumventing systemic side effects.

MicroRNA-207 enhances radiation-induced apoptosis by directly targeting Akt3 in cochlea hair cells.

MicroRNAs (miRNAs) have important roles in various types of cellular biological processes. Our study aimed to determine whether miRNAs function in the regulation of ionizing radiation (IR)-induced cell death in auditory cells and to determine how they affect the cellular response to IR. Microarray and qRT-PCR were performed to identify and confirm the differential expression of miRNAs in the cochlea hair cell line HEI-OC1 and in vivo after IR. Upregulation or downregulation of miRNAs using miRNA mimics or inhibitor were detected to characterize the biological effects of the indicated miRNAs. Bioinformatic analyses, luciferase reporter assays and mRNA knockdown were performed to identify a miRNA target gene. We determined that miR-207 was significantly upregulated after IR. MiR-207 enhances IR-induced apoptosis and DNA damage in HEI-OC1 cells. Furthermore, Akt3 was confirmed to be a direct target of miR-207. Downregulation of Akt3 mimics the effects of miR-207. MiR-207 enhances IR-induced apoptosis by directly targeting Akt3 and anti-miR-207 may have a potential role in protecting cochlea hair cells from IR.

Inhibition of p38 mitogen-activated protein kinase ameliorates radiation-induced ototoxicity in zebrafish and cochlea-derived cell lines.

Radiation is a widely used treatment for head and neck cancers, and one of its most severe side effects is ototoxicity. Radiation-induced ototoxicity has been demonstrated to be linked to the increased production of ROS and MAPK. We intended to investigate the effect of p38 inhibition on radiation-induced ototoxicity in cochlea-derived HEI-OC1 cells and in a zebrafish model. The otoprotective effect of p38 inhibition against radiation was tested in vitro in the organ of Corti-derived cell line, HEI-OC1, and in vivo in a zebrafish model. Radiation-induced apoptosis, mitochondrial dysfunction, and an increase of intracellular NO generation were demonstrated in HEI-OC1 cells. The p38-specific inhibitor, SB203580, ameliorated radiation-induced apoptosis and mitochondrial injury in HEI-OC1 cells. p38 inhibition reduced radiation-induced activation of JNK, p38, cytochrome c, and cleavage of caspase-3 and PARP in HEI-OC1 cells. Scanning electron micrography showed that SB203580 prevented radiation-induced destruction of kinocilium and stereocilia in zebrafish neuromasts. The results of this study suggest that p38 plays an important role in mediating radiation-induced ototoxicity and inhibition of p38 could be a plausible option for preventing radiation ototoxicity.

Radiation-induced Cochlea hair cell death: mechanisms and protection.

Cochlea hair cell death is regarded to be responsible for the radiation-induced sensorineural hearing loss (SNHL), which is one of the principal complications of radiotherapy (RT) for head and neck cancers. In this mini- review, we focus on the current progresses trying to unravel mechanisms of radiation-induced hair cell death and find out possible protection. P53, reactive oxygen species (ROS) and c-Jun N-terminal kinase (JNK) pathways have been proposed as pivotal in the processes leading to radiation hair cell death. Potential protectants, such as amifostine, N-acetylcysteine (NAC) and epicatechin (EC) , are claimed to be effective at reducing radiation- inducedhair cell death. The RT dosage, selection and application of concurrent chemotherapy should be pre- examined in order to minimize the damage to cochlea hair cells.

Effect of low-level laser treatment on cochlea hair-cell recovery after ototoxic hearing loss.

The primary cause of hearing loss includes damage to cochlear hair cells. Low-level laser therapy (LLLT) has become a popular treatment for damaged nervous systems. Based on the idea that cochlea hair cells and neural cells are from same developmental origin, the effect of LLLT on hearing loss in animal models is evaluated. Hearing loss animal models were established, and the animals were irradiated by 830-nm diode laser once a day for 10 days. Power density of the laser treatment was 900 mW/cm(2), and the fluence was 162 to 194 J. The tympanic membrane was evaluated after LLLT. Thresholds of auditory brainstem responses were evaluated before treatment, after gentamicin, and after 10 days of LLLT. Quantitative scanning electron microscopic (SEM) observations were done by counting remaining hair cells. Tympanic membranes were intact at the end of the experiment. No adverse tissue reaction was found. On SEM images, LLLT significantly increased the number of hair cells in middle and basal turns. Hearing was significantly improved by laser irradiation. After LLLT treatment, both the hearing threshold and hair-cell count significantly improved.

[Possible outer hair cells hazards from occupational exposure to very low frequency electric and magnetic fields: a pilot study].

OBJECTIVE: Our purpose was to investigate occupational high-strength very low frequency electric and magnetic fields (VLF EMFs) and assess changes of function of the inner ear. METHOD: The people exposed to high-strength VLF EMFs were divided into three groups: long- term exposure group ( > 5 years), short-term exposure group (< 5 years) and the control group. The field intensity indicator and noise analyzer were employed for the examination of the electromagnetic energy intensity and noise value at the working sites. Self-administered questionnaire was adopted. Universal hearing screening by pure tone audiometry (PTA) and distortion product otoacoustic emission (DPOAE) were done. The subjects who failed the screening tests were confirmed with auditory brainstem response (ABR) test. RESULT: The frequency of the electromagnetic field was 20 kHz, the average electric power density in job locations was 21-38 kV/m, which was higher than national standard (< 5 kV/m). Average noise-level in job locations was 52-65 dBHL, which was within the standard. Questionnaire presented that VLF EMFs might increase the incidence of headache, insomnia and tinnitus in long-term exposure. The incidence of abnormal DPOAE was higher in the subjects of the long-term exposure group than the short-term exposure group and the control group (P < 0.01). At 676, 933, 3616, 5130, 7253 Hz, the DPOAE amplitudes of the long term exposure group workers were significantly lower than the short-term exposure group and the control group. There was no obvious difference of the incidence of abnormal DPOAE between the short-term exposure group and the control group. The result of ABR with those subjects with abnormal DPOAE were no significant abnormalities. CONCLUSION: The average electric power density in job locations was significant worse than health standards. The changes of DPOAE indicated that the exposure to high-strength VLF EMFs had a subtle, discreet and localized impairing effect on outer hair cells. Effective intervention measures should be taken.

Effect of low-level laser therapy on cochlear hair cell recovery after gentamicin-induced ototoxicity.

Cochlear hair cells are the sensory receptors of the auditory system. It is well established that antibiotic drugs such as gentamicin can damage hair cells and cause hearing loss. Rescuing hair cells after ototoxic injury is an important issue in hearing recovery. Although many studies have indicated a positive effect of low-level laser therapy (LLLT) on neural cell survival, there has been no study on the effects of LLLT on cochlear hair cells. Therefore, the aim of this study was to elucidate the effects of LLLT on hair cell survival following gentamicin exposure in organotypic cultures of the cochlea of rats. The cochlea cultures were then divided into a control group (n = 8), a laser-only group (n = 8), a gentamicin-only group (n = 8) and a gentamicin plus laser group (n = 7). The control cultures were allowed to grow continuously for 11 days. The laser-only cultures were irradiated with a laser with a wavelength of 810 nm at 8 mW/cm(2) for 60 min per day (0.48 J/cm(2)) for 6 days. The gentamicin groups were exposed to 1 mM gentamicin for 48 h and allowed to recover (gentamicin-only group) or allowed to recover with daily irradiation (gentamicin plus laser group). The hair cells in all groups were stained with FM1-43 and counted every 3 days. The number of hair cells was significantly larger in the gentamicin plus laser group than in the gentamicin-only group. The number of hair cells was larger in the laser-only group than in the control group, but the difference did not reach statistical significance. These results suggest that LLLT may promote hair cell survival following gentamicin damage in the cochlea. This is the first study in the literature that has demonstrated the beneficial effect of LLLT on the recovery of cochlear hair cells.

Epicatechin inhibits radiation-induced auditory cell death by suppression of reactive oxygen species generation.

Radiation-induced toxicity limits the delivery of high-dose radiation to head and neck lesions. The aim of this study was to investigate the effectiveness of epicatechin (EC), a minor component of green tea extract, on radiation-induced ototoxicity in vitro and in vivo. The effect of EC on radiation-induced cytotoxicity was analyzed in the organ of Corti-derived cell lines, HEI-OC1 and UB-OC1. The cell viability, apoptosis, reactive oxygen species generation, and mitochondrial membrane potential as well as changes in the signal pathway related to apoptosis were investigated. Then, the therapeutic effects of hearing protection and drug toxicity of EC were explored in a zebrafish and rat model. Radiation-induced apoptosis and altered mitochondrial membrane potential in HEI-OC1 and UB-OC1 were observed. EC inhibited radiation-induced apoptosis and intracellular reactive oxygen species generation. EC markedly attenuated the radiation-induced embryotoxicity and protected against radiation-induced loss and changes of auditory neuromast in the zebrafish. In addition, intratympanic administration of EC was protective against radiation-induced hearing loss in the rat model, as determined by click-evoked auditory brainstem (P<0.01). EC significantly reduced the expression of p-JNK, p-ERK cleaved caspase-3, and cleaved PARP compared to their significant increase after radiation treatment. The results of this study suggest that EC significantly inhibited radiation-induced apoptosis in auditory hair cells and may be a safe and effective candidate treatment for the prevention of radiation-induced ototoxicity.

12th Yahya Cohen Memorial Lecture: The cellular and molecular basis of radiation-induced sensori-neural hearing loss.

INTRODUCTION: Sensori-neural hearing loss (SNHL) is a frequent complication of conventional radiotherapy for head and neck tumours, especially nasopharyngeal carcinoma. To manage radiation-induced ototoxicity appropriately, an understanding of the cellular and molecular basis of this complication is necessary. MATERIALS AND METHODS: A medline search of relevant literature was done, focusing on the radiation-induced cellular and molecular processes that lead to hair cell death in the cochlea. RESULTS: Radiation-induced SNHL occurs in the cochlea, with the retro-cochlear pathways remaining functionally intact. By simulating radiotherapy regimes used clinically, radiation-induced cochlear cell degeneration in the absence of damage to the supporting structures and blood vessels has been demonstrated in animals. This could be due to apoptotic cochlear cell death, which has been shown to be associated with p53 upregulation and intra-cellular reactive oxygen species (ROS) generation. Oxidative stress may initiate the upstream processes that lead to apoptosis and other cell death mechanisms. CONCLUSIONS: A model of radiation-induced SNHL based on a dose and ROS-dependent cochlear cell apoptosis, is proposed. This model supports the feasibility of cochlear implantation, should one be clinically indicated. It can explain clinical observations such as radiation-induced SNHL being dose-dependent and affects the high frequencies more than the lower frequencies. It also opens up the possibility of preventive strategies targeted at different stages of the apoptotic process. Antioxidants look promising as effective agents to prevent radiation-induced ototoxicity; they target upstream processes leading to different cell death mechanisms that may co-exist in the population of damaged cells.

Characterization of biological effect of 1763 MHz radiofrequency exposure on auditory hair cells.

PURPOSE: Radiofrequency (RF) exposure at the frequency of mobile phones has been reported not to induce cellular damage in in vitro and in vivo models. We chose HEI-OC1 immortalized mouse auditory hair cells to characterize the cellular response to 1763 MHz RF exposure, because auditory cells could be exposed to mobile phone frequencies. MATERIALS AND METHODS: Cells were exposed to 1763 MHz RF at a 20 W/kg specific absorption rate (SAR) in a code division multiple access (CDMA) exposure chamber for 24 and 48 h to check for changes in cell cycle, DNA damage, stress response, and gene expression. RESULTS: Neither of cell cycle changes nor DNA damage was detected in RF-exposed cells. The expression of heat shock proteins (HSP) and the phosphorylation of mitogen-activated protein kinases (MAPK) did not change, either. We tried to identify any alteration in gene expression using microarrays. Using the Applied Biosystems 1700 full genome expression mouse microarray, we found that only 29 genes (0.09% of total genes examined) were changed by more than 1.5-fold on RF exposure. CONCLUSION: From these results, we could not find any evidence of the induction of cellular responses, including cell cycle distribution, DNA damage, stress response and gene expression, after 1763 MHz RF exposure at an SAR of 20 W/kg in HEI-OC1 auditory hair cells.

Effects of prolonged exposure to an augmented acoustic environment on the auditory system of middle-aged C57BL/6J mice: cochlear and central histology and sex differences.

Genetic progressive sensorineural hearing loss in mice of the C57BL/6J (B6) inbred strain begins at high frequencies during young adulthood and is severe by 12 months (middle age). Nightly treatment with an augmented acoustic environment (AAE)--12-hour periods of exposure to repetitive noise bursts of moderate intensity, begun at age 25 days--resulted in less severe hearing loss compared with control mice. Cochlear histopathological correlates of AAE treatment, assessed at 12-14 months of age, included lessened severity of progressive loss of outer hair cells in both sexes as well as small savings of spiral ganglion cells in females and inner hair cells in males. AAE effects on the number of surviving neurons (age 12-14 months) in the anterior ventral cochlear nucleus (AVCN) depended on sex. Compared with controls, the loss of AVCN neurons that typically accompanies the initial period of hearing loss (between 2 and 7 months of age) was not significantly affected by AAE treatment in females. In contrast, males treated with the AAE exhibited more severe loss of neurons in the dorsal and ventral extremes of the AVCN than male controls of the same age. AAE treatment begun at age 3-5 months resulted in significant but less severe loss of AVCN neurons in 1-year-old male mice.

Effects of exposure of the ear to GSM microwaves: in vivo and in vitro experimental studies.

The effects of mobile phone (GSM) microwaves on the ears of guinea pigs were investigated in two in vivo experiments and one in vitro experiment. In the first experiment, three groups of eight guinea pigs had their left ear exposed for 1 h/day, 5 days/week, for 2 months, to GSM microwaves (900 MHz. GSM modulated) at specific absorption rates (SARs) of 1, 2 and 4 W/kg respectively, and a fourth group was sham-exposed. Distortion-product otoacoustic emissions (DPOAEs) were measured for each ear before exposure, at the end of the 2-month exposure period, and 2 months later. In the second experiment, the same protocol was applied to eight sham-exposed and 16 exposed guinea pigs at 4W/kg, but the auditory brainstem response (ABR) thresholds were monitored. Repeated-measures ANOVA showed no difference in DPOAE amplitudes or in ABR thresholds between the exposed and non-exposed ears and between the sham-exposed and exposed groups In the course of the second experiment, acute effects were also investigated by measuring once, in all animals, ABR thresholds just before and just after the 1-h exposure: no statistically significant difference was observed. In vitro, the two organs of Corti (OCs) of newborn rats (n=15) were isolated and placed in culture. For each animal, one OC was exposed for 24-48 h to 1 W/kg GSM microwaves, and the other was sham-exposed. After 2-3 days of culture, all OCs were observed under light microscopy. They all appeared normal to naive observers at this stage of development. These results provided no evidence that microwave radiation, at the levels produced by mobile phones, caused damage to the inner ear or the auditory pathways in our experimental animals.

Photoresponse from the statocyst hair cell in Lymnaea stagnalis.

Sensory cells for associative learning of light and turbulence were studied in Lymnaea. Intracellular recordings with Lucifer Yellow filled electrodes were made from photoreceptors and statocyst hair cells. Photoreceptors had a long latency, graded depolarizing response to a flash of light; they extended their axon to the cerebral ganglion. The caudal hair cell, one of 12 cells in the statocyst, responded to brief light with a depolarization and superimposed impulse activity. It formed its terminal arborization close to the photoreceptor endings in the cerebral ganglion. Ca(2+)-free saline reversibly abolished the photoresponse in the hair cell, suggesting the information was conveyed via a chemical synapse. These findings demonstrated that sensory information for associative learning was convergent at the statocyst hair cell.

[Enzyme histochemistry study of non-focused ultrasound irradiating the cochlea in guinea pigs].

OBJECTIVE: To study the enzyme histochemistry changes of non-focused ultrasound (NFU) irradiating the cochlea in guinea pigs. METHODS: After 30 minutes or 8 hours of 2.5 MHz, 8 MHz NFU irradiating the cochlea in guinea pigs (70 ears) for 6 hours, the SDH activity of the hair cells of the cochlea was observed. RESULTS: The non-focused ultrasound (2.5 MHz or 8 MHz) irradiation for 6 hours has lad to enervation of the activity of SDH in hair cells, especially in outer hair cells, in the 0.87 +/- 0.20 mm areas of the second turn or in the 0.80 +/- 0.20 mm areas of the first turn, respectively. The activity of SDH can be part restorable in the 8 hours groups. CONCLUSION: NFU (2.5 MHz, 8 MHz) irradiating the cochlea for 6 hours can cause pathological changes in the hair cells of in different areas of cochlear. Moreover, the pathological changes could be restorable or part restorable in some amounts of NFU irradiation. The results suggest that the cochlear hair cell of the different area might be related to ultrasonic perception.