BACKGROUND AND OBJECTIVES: Endolymphatic hydrops has been considered as an important histologic substrate of Meniere's disease. A permanent displacement of basilar membrane (BM) by increased endolymphatic pressure has been thought to be an explanation for hearing change. Direct observation of histological sections of temporal bones, however, suggested that stereocilia and tectorial membrane decoupling is more associated with pressure induced by mechanical deformation of the organ of Corti rather than with the displacement of BM. METERIALS AND METHOD: 26 cochleae from 13 female pigmented ginea pigs were harvested. One cochlea per each animal was injected with artificial perilymph. The other one was used as control. After fixation, followed by embedding and mid-modiolar sectionning, specimens were observed with a microscope. Morphometric parameters of each row and turn of the organ of Corti were measured and quantified. RESULTS: The average area and height of the organ of Corti were significantly smaller in the apical turn of the experimental group (p<0.05). The lengths of outer hair cell and Deiters cell in the apical turn were also significantly reduced in the experimental group (p<0.05). The angle between the outer hair cell and Deiters cell was smaller in the apex and in the 3rd turn of the experimental group (p<0.05). CONCLUSION: Results show that compression and deformation of the organ of Corti, especially in the apical turn, is a prominent feature in the acute endolymphatic hydrops model. We suggest that the deformation of organ of Corti is the primary cause of hydrops that induce the decoupling of tectorial membrane and stereocilia rather than the displacement of BM.
Animals ; Basilar Membrane ; Cochlea ; Edema ; Endolymphatic Hydrops* ; Female ; Guinea Pigs ; Hair ; Hearing ; Humans ; Meniere Disease ; Organ of Corti* ; Perilymph ; Stereocilia ; Swine ; Tectorial Membrane ; Temporal Bone

Mass and stiffness affect on the peculiar characteristics of transmission of the middle ear and the distinctive behavior of the cochlear mechanics. Applying the principle of the mass and stiffness, the band-pass characteristic transfer function of the middle ear has been explained. The greatest transfer function of the middle ear, approximately 24-29 dB, is observed at 1-2 kHz in both cat and human species. However, at lower frequencies, the transfer function was disturbed by the stiffness of the middle ear primarily due to middle ear cavity. At higher frequencies, the transfer function was disturbed by the stiffness of the middle ear primarily due to middle ear bones. Several examples, such as an acoustic reflex, otitis media, and otosclerosis are discussed. For understanding the traveling wave of the basilar membrane, different place tuning at certain stimulus frequencies, contrastingly shaped basilar membrane to the cochlear duct, and the structural and physical characteristics of the whole cochlear partition were reviewed in terms of changing width, mass, and stiffness from the base to apex. Being about ten times wider, more massive, and one hundredfold stiffer at the base than the apex, the nature of the cochlear partition to absorb high-frequency energy changes in fluid pressure declines toward the apex. Consequently, at the base of the cochlea, high frequencies stimuli are decoded while low frequencies stimuli are decoded at the apex of the cochlea. Due to these characteristics of the cochlear partition, the direction of the traveling wave was also proved to be in the fashion of base-to-apex always.
Animals ; Basilar Membrane ; Cats ; Cochlea ; Cochlear Duct ; Ear, Middle* ; Humans ; Mechanics ; Otitis Media ; Otosclerosis ; Reflex, Acoustic

OBJECTIVE: To study the relationship of distortion product in cochlea with cochlear activity and hearing. METHOD: Time variances of distortion product of basilar membrane vibration in vitro guineapig cochlea were observed by laser interferometry. RESULT: Within half hour after a cochlea was isolated from a guineapig, distortion product accompanied with two-tone inhibition in cochlea, can be observed. As time passed, distortion product and two-tone inhibition effect disappeared at the same time. After that, the membrane contiune vibrating in response to the sound stimulus, but the vibration amplitude decreased obviously and continued decreasing until it disappeared completely. CONCLUSION Distortion product in cochlea is a symbol of cochlear activity which makes the membrane respond in large amplitude vibration to sound stimulus and exhibit two-tone inhibition. The former makes the hearing highly sensitive to sound stimulus, the later makes the hearing perform information abstract well.
Acoustic Stimulation ; Animals ; Basilar Membrane ; physiology ; Cochlea ; physiology ; Guinea Pigs ; Hearing ; physiology ; Hearing Tests ; Interferometry ; Sound

OBJECTIVETo establish a mechanical simulation model for studying the relationship between the characteristic frequency and feature location of the basilar membrane of the cochlea.

METHODSMacro-mechanical methods were used to simplify the details of the model. With simulation tools, the basilar membrane vibration frequency characteristics were analyzed based on the box model.

RESULTSThe basilar membrane had obvious frequency-selective properties, and the basilar membrane from the stapes was sensitive to high frequencies while the farther membrane was sensitive to low frequencies.

CONCLUSIONThe frequency characteristics of the basilar membrane of the cochlea is mainly a result of the longitudinal variations of the geometric dimensions and material properties and is not related with other structures within the cochlea corti.

Spontaneous, rhythmical contractions, or vasomotion, can be recorded from cerebral vessels under both normal physiological and pathophysiological conditions. We investigated the cellular mechanisms underlying vasomotion in the cerebral basilar artery (BA) of Wistar rats. Pressure myograph video microscopy was used to study the changes in cerebral artery vessel diameter. The main results of this study were as follows: (1) The diameters of BA and middle cerebral artery (MCA) were 314.5±15.7 μm (n=15) and 233.3±10.1 μm (n=12) at 10 mmHg working pressure (P<0.05), respectively. Pressure-induced vasomotion occurred in BA (22/28, 78.6%), but not in MCA (4/31, 12.9%) from 0 to 70 mmHg working pressure. As is typical for vasomotion, the contractile phase of the response was more rapid than the relaxation phase; (2) The frequency of vasomotion response and the diameter were gradually increased in BA from 0 to 70 mmHg working pressure. The amplitude of the rhythmic contractions was relatively constant once stable conditions were achieved. The frequency of contractions was variable and the highest value was 16.7±4.7 (n=13) per 10 min at 60 mmHg working pressure; (3) The pressure-induced vasomotion of the isolated BA was attenuated by nifedipine, NFA, 18β-GA, TEA or in Ca(2+)-free medium. Nifedipine, NFA, 18β-GA or Ca(2+)-free medium not only dampened vasomotion, but also kept BA in relaxation state. In contrasts, TEA kept BA in contraction state. These results suggest that the pressure-induced vasomotion of the isolated BA results from an interaction between Ca(2+)-activated Cl(-) channels (CaCCs) currents and K(Ca) currents. We hypothesize that vasomotion of BA depends on the depolarizing of the vascular smooth muscle cells (VSMCs) to activate CaCCs. Depolarization in turn activates voltage-dependent Ca(2+) channels, synchronizing contractions of adjacent cells through influx of extracellular calcium and the flow of calcium through gap junctions. Subsequent calcium-induced calcium release from ryanodine-sensitive stores activates K(Ca) channels and hyperpolarizes VSMCs, which provides a negative feedback loop for regenerating the contractile cycle.
Animals ; Basilar Artery ; cytology ; metabolism ; physiology ; Chloride Channels ; metabolism ; Female ; Male ; Membrane Potentials ; physiology ; Muscle, Smooth, Vascular ; cytology ; metabolism ; Myocytes, Smooth Muscle ; cytology ; metabolism ; Potassium Channels, Calcium-Activated ; metabolism ; Rats ; Rats, Wistar ; Vasoconstriction ; physiology ; Vasodilation ; physiology

OBJECTIVES: Apoptosis may play an important role in the mechanism underlying the GJB2 gene conditional knockout (cCx26) mice cochlear cell death. The objective of this study was to explore the the damage mode of the outer hair cells (OHCs) and its real time point of apoptosis and provide information to further explore the role of apoptosis in the happening of hearing loss in cCx26 mice. METHODS: Cochleae from mice at various developmental stages (P8, P12, and P21) were dissected out and first used to be observed under the scanning electron microscope (SEM). Basilar membranes from mice at P8, P14, P18, and P21 were stained by fluorescein isothiocyanate-conjugated phalloidin and propidium iodide (PI) and examined under confocal microscope. RESULTS: The loss of OHCs of cCx26 knockout mice was first set between P12 and P21 under SEM. Whole mount phalloidin and PI staining revealed that obvious apoptotic appearance of the OHCs surface morphology was observed at P18. CONCLUSION: Typical apoptotic morphology was found in the OHCs in the organ of Corti of the cCx26 mice at P18. This may provide information to further study the role of apoptosis in the occurrence of hearing loss of cCx26 mice.
Animals ; Apoptosis ; Basilar Membrane ; Cell Death ; Cochlea ; Connexins ; Electrons ; Fluorescein ; Hair ; Hair Cells, Auditory, Outer ; Hearing Loss ; Hearing Loss, Sensorineural ; Mice ; Mice, Knockout ; Organ of Corti ; Phalloidine ; Propidium

The main objective of this study is to provide an overview of the basic mechanisms of blast induced hearing loss and review pharmacological treatments or interventions that can reduce or inhibit blast induced hearing loss. The mechanisms of blast induced hearing loss have been studied in experimental animal models mimicking features of damage or injury seen in human. Blast induced hearing loss is characterized by perforation and rupture of the tympanic membrane, ossicular damage, basilar membrane damage, inner and outer hair cell loss, rupture of round window, changes in chemical components of cochlear fluid, vasospasm, ischemia, oxidative stress, excitotoxicity, hematoma, and hemorrhage in both animals and humans. These histopathological consequences of blast exposure can induce hearing loss, tinnitus, dizziness, and headache. The pharmacological approaches to block or inhibit some of the auditory pathological consequences caused by blast exposure have been developed with antioxidant drugs such as 2,4-disulfonyl alpha-phenyl tertiary butyl nitrone (HXY-059, now called HPN-07) and N-acetylcysteine (NAC). A combination of antioxidant drugs (HPN-07 and NAC) was administered to reduce blast induced cochlear damage and hearing loss. The combination of the antioxidant drugs can prevent or treat blast induced hearing loss by reducing damage to the mechanical and neural component of the auditory system. Although information of the underlying mechanisms and treatment of blast induced hearing loss are provided, further and deep research should be achieved due to the limited and controversial knowledge.
Acetylcysteine ; Animals ; Basilar Membrane ; Blast Injuries ; Dizziness ; Hair ; Headache ; Hearing ; Hearing Loss ; Hematoma ; Hemorrhage ; Humans ; Ischemia ; Models, Animal ; Oxidative Stress ; Rupture ; Tinnitus ; Tympanic Membrane

The main objective of this study is to provide an overview of the basic mechanisms of blast induced hearing loss and review pharmacological treatments or interventions that can reduce or inhibit blast induced hearing loss. The mechanisms of blast induced hearing loss have been studied in experimental animal models mimicking features of damage or injury seen in human. Blast induced hearing loss is characterized by perforation and rupture of the tympanic membrane, ossicular damage, basilar membrane damage, inner and outer hair cell loss, rupture of round window, changes in chemical components of cochlear fluid, vasospasm, ischemia, oxidative stress, excitotoxicity, hematoma, and hemorrhage in both animals and humans. These histopathological consequences of blast exposure can induce hearing loss, tinnitus, dizziness, and headache. The pharmacological approaches to block or inhibit some of the auditory pathological consequences caused by blast exposure have been developed with antioxidant drugs such as 2,4-disulfonyl alpha-phenyl tertiary butyl nitrone (HXY-059, now called HPN-07) and N-acetylcysteine (NAC). A combination of antioxidant drugs (HPN-07 and NAC) was administered to reduce blast induced cochlear damage and hearing loss. The combination of the antioxidant drugs can prevent or treat blast induced hearing loss by reducing damage to the mechanical and neural component of the auditory system. Although information of the underlying mechanisms and treatment of blast induced hearing loss are provided, further and deep research should be achieved due to the limited and controversial knowledge.
Acetylcysteine ; Animals ; Basilar Membrane ; Blast Injuries ; Dizziness ; Hair ; Headache ; Hearing ; Hearing Loss ; Hematoma ; Hemorrhage ; Humans ; Ischemia ; Models, Animal ; Oxidative Stress ; Rupture ; Tinnitus ; Tympanic Membrane

BACKGROUND AND OBJECTIVES: The diagnosis of Meniere's disease is based on audiological test and clinical symptoms. Cochlear Hydrops Analysis Masking Procedure (CHAMP) was introduced as a test for detecting changes in physical characteristics of basilar membrane by hydrops of endolympahtic system. The aim of this study is to evaluate the diagnostic value and usefulness of CHAMP tests for detection of endolymphatic hydrops. SUBJECTS AND METHOD: This study was performed on 11 cases of Meniere's disease and 10 cases of vestibular neuritis who visited ENT outpatient clinic and 25 cases of normal healthy volunteers. We defined the positive value as being less than 0.3 ms in latency delay (0.5 kHz HPN-click alone) and less than 0.95 nV in compound amplitude ratio (click alone 0.5 kHz HPN/ click alone) regardless of age or sex. RESULTS: There were significant latency delays in the Meniere's disease group compared with the vestibular neuritis and normal control group. The amplitude ratio gave significant differences between the Meniere's disease group and the normal group but there were no differences between the Meniere's disease group and the vestibular neuritis group. Without assuming the test failure, the sensitivity and specificity of latency delay was 81% and 100%, respectively, and the sensitivity and specificity of amplitude ratio was 100% and 84%, respectively. In 8 of 54 cases (14.8%), we couldn't get interpretable wave. CONCLUSION: CHAMP test is a clinically useful method that can detect endolymphatic hydrops and it can be used as an objective test for the diagonosis of Meniere's disease.
Ambulatory Care Facilities ; Basilar Membrane ; Edema ; Endolymphatic Hydrops ; Masks ; Meniere Disease ; Sensitivity and Specificity ; Vestibular Neuronitis

OBJECTIVE: To construct an adenoviral vector that codes for both human NT3 and EGFP, to confirm the transduction efficiency in rat cochlear cultures and to assess the protection of NT3 on SGNs survival. METHOD: PAdeasy-1 and pAdTrack CMV were used to constructed Ad/NT3 adenovirus and then to transfer postnatal day 3 rat cochlear cultures. The transduction efficiency was determined by microscope observation. The amounts of SGNs were counted to evaluated protection of Ad/NT3 on SGNs survival. RESULT: EGFP positive cells were observed in all cochlear turns. There was approximately 49% in outer sulcus cells and 27% in the interdental cells; less than 2% of the hair cells and SGN. The amounts of SGN of treated Ad/NT3 adenovirus are more than cochlea SGN only Ad/EGFP adenovirus after cultured for 15 days. CONCLUSION Ad/NT3 adenovirus could transduce EGFP and NT3 in large number of supporting cells, but few hair cells or SGNs. The putative release of NT3 from these supporting cells could enhance cell survival and promote neurite outgrowth from SGNs.
Adenoviridae ; genetics ; Animals ; Basilar Membrane ; cytology ; Cell Survival ; genetics ; Cells, Cultured ; Cochlea ; cytology ; Genetic Vectors ; Hair Cells, Auditory ; cytology ; Humans ; Neurotrophin 3 ; genetics ; Rats ; Rats, Inbred F344 ; Transfection