Direct precision frequency measurement and correction technology with double ADC.

A new method of direct precision frequency measurement is proposed in this paper, which uses the clock cursor effect between the sampling clock signal and input signal and ADC (analog to digital converter) quantization error suppression technique in the background of digital measurement with double ADC. On this basis, a precision frequency corrector is designed. Compared with the traditional frequency synthesizer, this device takes the non-standard frequency signal of the crystal oscillator as the reference to realize the standard frequency signal output through the frequency correction function. Meanwhile, the output signal is obviously narrower in range, from 0.0001 Hz to 0.1 Hz. The frequency corrector can also realize the second stability of less than 3 × 10-12 and a small frequency correction of 10-11 orders of magnitude.

Response of cochlear potentials to presumed alterations of ionic conductance: endolymphatic perfusion of barium, valinomycin and nystatin.

Two models ('single-pump' and 'two-pump') of transepithelial potassium movement by the marginal cells of the stria vascularis have been proposed in the literature. Their validity was considered by exposing the endolymphatic (luminal) surface to agents (barium, valinomycin and nystatin) which are known to alter specific cellular membrane conductances in other tissues. This was accomplished by the use either of injections or of a relatively satisfactory technique for perfusion of scala media, which is described. Injection of barium caused the endocochlear potential (EP) to increase in normal animals and had no effect on the EP of deaf, Waltzing guinea pigs. Perfusion of the ionophores caused a decline in the EP in both normal and Waltzing guinea pigs. Only the 'two-pump' model (Na/K-ATPase-mediated cation pump on the basolateral membrane and rheogenic K transporter at the luminal membrane) is consistent with the results. The cellular heterogeneity of the cochlear duct, however, introduces a measure of uncertainty into this interpretation.

The pathophysiology of compression injuries of the peripheral facial nerve.

The buccolabial branches of guniea pig facial nerves were crushed to produce axonotmesis, Wallerian degeneration, and demyelination. The lesions were followed from 1 to 8 weeks by transmission electron microscopy, electrophysiological tests, and cytochemical staining methods for Na+ channels. The first week demonstrated the classic degenerative neural changes. At 2 weeks the axoplasmic side of the demyelinated axolemma demonstrated diffuse staining for Na+ channels at a distance of 1 micrometer. At 4 weeks multiple condensed areas of dense staining were noted along the demyelinated axolemma. These staining areas resemble in character and length a normal node of Ranvier and denote new Na+ channels. The internodal distance is shorter than for the normal facial nerve. At 6 weeks a thin layer of myelin covered the nerve fibers. At 8 weeks half of the nerves were normal sized and the myelin sheath was normal in width. Following nerve crushing, electrical activity is present for 24-48 hours in the axonotmetic distal stump. Then the axon becomes unresponsive to electrical stimulation. There is gradual resumption of electrical activity between 5 and 14 days. Normal conduction resumes by 8 weeks. This study provides ultrastructural and cytochemical evidence for nerve fiber reorganization, axolemmal plasticity and sodium channel production and redistribution following Wallerian degeneration and demyelination in axonotmesis. Resumption of electrical neural excitability is achieved by an increase in the density of sodium channels and reduction in the internodal distance as a means for impedence matching. Reduction of the cross sectional diameter of the regenerating axon facilitates electrical conduction.

Comparison of the non-adrenergic action of phentolamine with that of vanadate on cochlear function.

Two drugs, which upon superficial examination appeared to be acting on common processes, have been found upon closer investigation to act by quite different means. Both act primarily at the organ of Corti, causing a pronounced increase of the endocochlear potential and a depression of the cochlear microphonic (CM). These effects are accompanied by the elimination of a negative component of the EP; however, it was found that these three effects are produced by phentolamine in scala media (or, more slowly, in scala tympani) but by vanadate only in scala tympani. This difference in locus of action isd manifested further by different changes of the summating potential (SP): phentolamine has little effect on the magnitude of SP-, while vanadate leads to an elevated SP-. In spite of this difference in the 'zeroth order harmonic', the second harmonic of the CM is depressed by both agents. It is argued that phentolamine may act either by blocking the acoustically-modulated ion channels in the luminal membranes of the hair cells or by inducing a large, non-selective, paracellular conductance in the organ of Corti. The present results, in conjunction with our previous results (Marcus, D.C., DeMott, J.E., Kobayashi, T., Ge, X.-X. and Thalmann, R. (1981): Hearing Res. 5, 231-243), are further interpreted as suggesting that vanadate may initially act by depolarizing the hair cells.

Specificity of action of vanadate to the organ of corti.

Although vanadate strongly inhibits Na/K-ATPase activity of the stria vascularis in vitro, it initially causes no depression of the ouabain-sensitive endocochlear potential (EP) when perfused perilymphatically or via the vasculature. However, when the perilymph of scala tympani is replaced with artificial media containing 0.1 to 1 mM vanadate, there is a large (about 17 mV) increase in the EP of the second cochlear turn. Further experiments showed that the cochlear microphonics declined during the time in which the EP increased, and that the response of these two potentials to vanadate is greater in the second turn than in the first. Injection of 50 n1 of 1 mM vanadate (in artificial endolymph) into the endolymphatic space of the second turn caused no increase in the EP. These results support the notion that the early effects of vanadate are on the contra-luminal membranes of cells of the organ of Corti rather than on the stria vascularis. By superimposing anoxia or furosemide (i.v.) upon vanadate intoxication, we determined that the initial increase of the compound EP due to vanadate alone was due to a reduction in magnitude of the negative component of the EP. It is argued that of the three prevalent theories concerning the generation of the negative EP, the data tend to support the hypothesis that the intracellular potential of the hair cells gives rise to the negative EP.

Development of the hypotympanum in the human fetus and neonate.

The human hypotympanum develops over a 10-week period in utero (22-32 weeks) as a triphasic osseous mosaic. The tympanic bone ossifies as a membranous bone (8-36 weeks in utero). The canalicular otic capsule ossifies in cartilage by 26 weeks in utero. A petrosal ledge of bone ossifies as periosteal bone at 24-29 weeks in utero. The fusion of these three bony structures closes the hypotympanum and forms two persistent hypotympanic fissures. The medial hypotympanic fissure forms between the canalicular otic capsule and petrosa at 24 weeks in utero. It transmits the medial hypotympanic artery and vein (from the posterior CNS circulation) and Jacobson's nerve (from the ninth nerve). The lateral hypotympanum fissure forms between the tympanic bone and the petrosa at 29 weeks in utero. It transmits the lateral hypotympanic artery and vein from the external carotid circulation. The two vascular supplies form a rich hypotympanic plexus on the floor of the middle ear. The fibrous annulus and middle layer of the tympanic membrane form an avascular plane.

Labyrinthine segment and geniculate ganglion of facial nerve in fetal and adult human temporal bones.

The later stages of development (15-40 weeks in utero) of the geniculate ganglion and labyrinthine segment of the facial nerve in the human fetus demonstrate minimal neuronal growth. The vascular supply is well established. The major changes occur in the perineural ossification pattern. The canal of the labyrinthine facial nerve segment ossifies first via the petrous apex and periotic capsule. The narrowest portion of the canal is at the geniculate ganglion in the earlier stages and at the fundus of the internal auditory canal at term. The geniculate ganglion area ossifies by means of two bony plates. The medial plate is a derivate of the periosteal growth of the petrous apex and the lateral plate is an extension of membranous bone from the squama. The major relationships to the middle ear do not change. The hiatus of the facial canal diminishes in size during gestation, but remains patent at birth.