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At least 1,135 records · Page 63Linked to original sources
PubMed1979

Effects of noise on cochlear potentials and endolymph potassium concentration recorded with potassium-selective electrodes.

Guinea pig cochleas were exposed to either broad-band noise at intensities between 95 and 115 dBA or octave-band noise centered at 380 Hz or 4.2 kHz at intensities between 115 and 125 dB SPL. Cochlear microphonics (CM), summating potentials (SP) and action potentials (AP) were recorded from differential electrodes in the perilymphatic scalae between successive 20-min periods of noise exposure. The endocochlear potential (EP) and endolymph potassium concentration [Kendo+] were recorded continuously from scala media using double-barreled potassium-sensitive electrodes. It was found that the initial exposure to noise at 115 dBA produced considerable suppression of the CM and AP, while the EP and [Kendo+] were elevated above their normal values. When animals previously treated with kanamycin were subjected to the same level of noise exposure no systematic increase in either EP ro [Kendo+] was observed. After prolonged exposure to 380 Hz octave-band noise at 125 dB SPL, a slow decline of EP and [Kendo+] was observed. The relationships between the changes in EP, [Kendo+] and CM are discussed.

Animals↗
PubMed1981

[Kanamycin-induced lesions of the stria vascularis: preliminary results of an electrophysiological and ultrastructural study (author's transl)].

Ten guinea-pigs were treated with kanamycin 400 mg/kg for a 10-day period. Electrophysiological investigations were carried out, and the animals were killed one month after the end of the treatment for electron microscope study of the second turn of the cochlear spiral. The microphonic potential was considerably reduced, and the stria vascularis was the seat of lysosomal inclusions in the marginal and intermediate cells associated with myeloid bodies in the vascular endothelium. There was a gradient of lysosomal catabolic residues, probably lipoproteins, from the vascular sector to the cochlear canal; some of these products passed into the cochlear canal. Alterations of the hair cells in the second spire appeared to be minimal. It is hypothesized that damage to the stria vascularis precedes damage to the hair cells.

Animals↗
PubMed1996

Changes in CM and CAP with sedation and temperature in the guinea pig: facts and interpretation.

The influence of xylazine on the amplitude, latency and waveform of VIIIth nerve compound action potential (CAP) and cochlear microphonic (CM) in response to clicks at 95 dB SPL in normal awake preimplanted guinea pigs was investigated. The animals' temperature was monitored but no thermoregulation was exerted, except in one control experiment. Following a 0.2 ml injection of xylazine, CM showed minor variations while CAP audiograms for tone pips between 0.5 and 25 kHz remained normal. However, a progressive decrease in temperature and a strongly correlated increase in CAP amplitude and in N1 and N2 latencies were noticed. For peak N1 the changes were equivalent to linear amplitude and time expansions, and could be reproduced through CAP synthesis with convolution methods using time expanded unit response model and firing density functions. All changes were maximal after 2 h of sedation and recovered within approximately another 2 h. Whereas xylazine is known to induce hypothermia, all the changes disappeared if the animal was thermoregulated. Therefore the changes are interpreted as a result of hypothermia. The mechanism of N1 latency lengthening and increase in amplitude during hypothermia can be understood as a simultaneous increase in spike duration, hair cell/nerve synaptic delay and postsynaptic time constant. This hypothesis yielded a theoretical temperature coefficient for N1 latency (-52 microseconds/degree C) matching that measured experimentally (-55 microseconds/degree C). When compared with peak N1, peak N2 appeared relatively more expanded. Arguments about the origin of N2 are discussed.

Acoustic Stimulation↗
PubMedDate not supplied

Increased fatigue of cochlear potentials after injection of KCl solution in the perilymph.

Cochlear microphonics (CM), action potentials (AP) and endochochlear potential (EP) were recorded on guinea pigs. The introduction of a small quantity of KCl solution (0.1 N) in the perilymph provoked a moderate decrease of CM and AP. During the period of depressed but stable amplitude, the presentation of intense sounds provoked an exaggerated susceptibility to fatigue and a delayed recovery. Similar changes were observed in the evolution of EP. However, the recovery was slower for EP than for CM. The results, as a whole, suggest that the fatigue which is manifested in the depression of cochlear potentials is related to a leakage of potassium ions from endolymph to fluids spaces within the organ of Corti.

Acoustic Stimulation↗
PubMed1981

The effects of frusemide, bumetanide and piretanide on the quinea pig cochlea and auditory nerve.

Frusemide, bumetanide and piretanide were introduced into scala tympani of the guinea pig cochlea by perfusion. The short-term effects of these drugs on the cochlear microphonic, the compound action potential and on the activity of single auditory nerve fibres were studied. the compound action potential was more sensitive to the action of the above compounds than was the cochlear microphonic. Single auditory nerve fibres showed a marked increase in threshold and generally a fall in spontaneous firing rate. A deterioration in in tuning was observed which in some cases, was not invariably accompanied by a rise in threshold. Histological examination revealed oedematous changes in stria vascularis and in supporting cells following cochlea perfusion with the above compounds.

Animals↗
PubMedDate not supplied

Ototoxicity of cis-dichlorodiammine platinum (II) in guinea pigs.

Effects of cis-dichlorodiammine platinum (II), an agent that has potent antineoplastic activity, were studied in guinea pigs. With repeated administration of a daily dose of 1.5 mg/kg of cis-dichlorodiammine platinum, the cochlear microphonics were suppressed. Suppression of the cochlear microphonics was greater in the basal turn than in the third turn of the cochlea. There was a close correlation between loss of the cochlear hair cells and suppression of the cochlear microphonics. The endocochlear potential was decreased in the basal turn but remained unchanged in the upper turn of the cochlea. The sodium, potassium, and chloride concentrations in both endolymph and perilymph were not affected. Slight and moderate congestion and regeneration of tubular epithelium of kidney were observed in guinea pigs treated with cis-dichlorodiammine platinum.

Animals↗
PubMedDate not supplied

Effect of glycerol on cochlea microcirculation.

Microcirculation in the cochlea of l2 normal anesthetized guinea pigs was investigated after intravenous infusion of 2.4 ml/kg of 40% glycerol. In these experiments endolymphatic PO2, blood pressure, cochlear microphonics, and endocochlear potentials were recorded. Administration of glycerol caused a significant increase in endocochlear PO2 for about 30 minutes. The improvement of hearing in patients with Meniere's disease is thus not only a result of the reduced hydrostatic pressure, as has been demonstrated by others, but may also be the result of vasodilatation, which improves microcirculation in the cochlea with resultant increases in endocochlear PO2.

Animals↗
PubMed1990

Effects of forskolin and 1,9-dideoxy-forskolin on cochlear potentials.

Endocochlear potential (EP) and cochlear microphonics (CM) were recorded during the perilymphatic perfusion with forskolin known as an adenylate cyclase stimulant. Forskolin produced a reversible EP elevation in a dose-dependent manner. Perfusion with 1,9-dideoxy-forskolin, an analogue of forskolin that does not stimulate adenylate cyclase, had no effect on EP, whereas perfusions with other agents that raise the cAMP-level (IBMX, a phosphodiesterase inhibitor, and dbcAMP) duplicated the effect of forskolin. The vigorous CM during the EP elevation and the large negative EP induced by anoxia superimposed on the elevated EP indicate that the K+ diffusion potential through the hair cell membrane cannot be altered by forskolin. The results suggest that the adenylate cyclase system in the stria vascularis and/or Reissner's membrane may modulate the generation of EP.

1-Methyl-3-isobutylxanthine↗
PubMed1966

Tetraethylammonium and tetrodotoxin: effects on cochlear potentials.

Tetraethylammonium chloride, which is believed to decrease potassium conductance, and tetrodotoxin, which apparently decreases sodium conductance in nerve fibers, were introduced iontophoretically into the organ of Corti or the scala media of guinea pig cochlea. The former depressed the direct-current endocochlear potential and also the alternating-current cochlear microphonics (the receptor potential of the ear), but tetrodotoxin was ineffective except on the nerve impulses.

Animals↗
PubMed1981

Effects of hypothermia on ionic movement in the guinea pig cochlea.

Anesthetized and immobilized guinea pigs were subjected to hypothermia. During cooling, the cochlear microphonics and endocochlear potential decreased and K+ concentrations in both endolymph and perilymph were not significantly affected. The rate constant for K+ turnover to endolymph was determined by uptake of 43K into the endolymph when the perilymphatic space was perfused with artificial perilymph containing 43K. The rate constant for K+ decreased significantly in hypothermic guinea pigs when compared with that in normal guinea pigs. The K+ conductance of the endolymph-perilymph barrier, estimated from the rate constant, showed a marked decrease in hypothermic guinea pigs and was comparable with the K+ conductance, calculated from the rate of change of the endolymph K+ concentrations relative to the K+ electrochemical potential difference, recorded during permanent anoxia. These results suggest that hypothermia not only suppresses the active K+ transport system but also decreases the K+ permeability of the endolymph-perilymph barrier.

Animals↗
PubMed1978

Bilateral recording of early auditory evoked responses in the cat.

The brain-stem electric responses of the cat evoked by a short 4 kHz tone burst have been differentially recorded between vertex and both ipsilateral and contralateral ear electrodes. Six vertex-positive waves can be recognised in both recordings. Animals with hereditary unilateral anacusis were studied in order to avoid cross-stimulation of the opposite ear. The cochlear microphonic and summating potential can be readily recorded in young animals, occur simultaneously in both tracings, and show polarity inversion at the contralateral electrode. The later neural potentials have the same polarity and practically identical latencies in the ipsilateral and contralateral recordings, whilst the first three brain-stem waves show approximate polarity inversion and variable latency relationships in the two recording situations. It is concluded that none of the brain-stem waves represents electric activity from a discrete generator.

Animals↗
PubMed1998

Trichloroethylene ototoxicity: evidence for a cochlear origin.

Trichloroethylene (TCE) is known to produce an unusual pattern of hearing impairment in laboratory animals marked by a preferential loss of threshold sensitivity at midfrequencies. The purpose of this research was to determine whether the TCE-induced auditory deficit results from cochlear dysfunction. Adult Long Evans hooded rats were exposed via inhalation to either 0 (clean air) or 4000 ppm TCE (6 h/day for 5 days). Auditory thresholds for 1-40 kHz tones were determined 3 weeks after exposure using reflex modification audiometry (RMA; n = 12/group). Cochlear electropotentials were measured during subsequent testing (n = 3-10/group) 5 to 7 weeks after exposure, including thresholds for cochlear action potentials (CAP) and the 1-microV cochlear microphonic for 2-40 kHz tones, and the N1 amplitude intensity function (40-90 dB SPL). Cochlear histopathology was assessed in midmodiolar preparations of a separate set of animals, exposed as before (n = 4/group). RMA testing confirmed a TCE-induced loss in midfrequency threshold sensitivity (8 and 16 kHz). CAP thresholds were elevated at midfrequencies (8 and 16 kHz) among TCE-treated subjects, along with a suppression of the N1 amplitude from 50 to 90 dB SPL. The cochlear microphonic, a nonpropagated ac potential generated largely by the outer hair cells, was not affected by the TCE treatment. Cochlear histopathology revealed a loss of spiral ganglion cells that was significant in the middle turn, but not in the basal turn. There was an inconsistent loss of hair cells among treated subjects. The data suggest strongly that the behaviorally determined loss in auditory function can be accounted for by a cochlear impairment and that the spiral ganglion cell may be a prominent target of TCE.

Animals↗
PubMed1985

Brainstem and cochlea potentials evoked by rarefaction and condensation single-slope stimuli. A preliminary report.

Influences of stimulus polarity on Jewett wave V are rather small when using clicks which produce two or more polarity changes within a short time interval. In order to separate pressure changes towards rarefaction (R) and towards condensation (C) we applied steep single-slope stimuli returning very slowly to baseline. Brainstem responses recorded from 8 human subjects differed markedly for R and C onset. Amplitudes were much higher for R than for C onset. The main C response was double-peaked with the first peak appearing about 0.5 ms earlier and the second, higher one, 1 ms later than the predominant R wave. The transition from single-slope to click stimulation was investigated by combining R and C slopes. For large time intervals, independent responses to either slope were observed. Down to an on/off interval of 1 ms, the on-response predominated. For still shorter intervals an equalization of R and C responses and a graduation towards click responses was found. Using the same stimuli, cochlear microphonics (CM) and compound action potentials (CAP) were recorded from 7 guinea pigs. The CM did not replicate the slow off-motion of the single-slope stimulus, but returned back to baseline after 0.6 ms. The C compared with R latency of the CAP (peak N1) was also delayed by 0.6 ms. This delay, and that of human peak V, may be explained by CAP initiation only by one direction of basilar membrane motion.

Acoustic Stimulation↗
PubMed1979

Effects of local application of ototoxic antibiotics on cochlear potentials in guinea pigs.

The effects of neomycin, kanamycin and dihydrostreptomycin on the cochlear microphonic, the action potential of the auditory nerve and the endocochlear potential were studied in guinea pigs in which these drugs were locally administered by perfusion. These drugs suppressed the cochlear responses markedly when applied to the endolymph but were less effective when applied to the perilymph. The mechanisms of action of antibiotics on the hair cells of the organ of Corti are discussed.

Action Potentials↗
PubMed1997

Effects of experimental cochlear thrombosis on oxygenation and auditory function of the inner ear.

To elucidate the etiology and pathogenesis of sudden hearing loss, the effect of experimental cochlear thrombosis on oxygenation and the auditory function of the inner ear was investigated in anesthetized guinea pigs. Impairment of cochlear blood flow (CBF) was induced by ferromagnetic obstruction of cochlear blood vessels at lowered body temperature. Perilymphatic oxygen partial pressure (PO2) in the basal scala tympani (about 200 microm below the round window membrane) was measured polarographically using micro-coaxial needle electrodes. Auditory function was examined by recording cochlear microphonic (CM) frequency responses, compound action potentials (CAP) and auditory evoked brainstem responses (ABR). Findings demonstrated a considerable decrease in the mean perilymphatic PO2 of 40%, 2 h after the start of the experiment. Mean CM and N1 CAP amplitudes were reduced by about 25% each and ABR by 18%. No significant changes were observed in the latencies of either CAP or ABR. Mean basal CBF was found to decrease by 35%, as measured by laser Doppler flowmetry in a parallel study. The present findings demonstrate that vascular impairment in the inner ear results in a considerable drop in intracochlear oxygenation, causing a significant loss in the auditory response.

Action Potentials↗
PubMed1988

2-Amino-4-phosphonobutyric acid receptors are not involved in synaptic transmission from hair cells to auditory neurons.

The chemical 2-amino-4-phosphonobutyric acid (APB, AP4), an excitatory amino acid antagonist, was perfused through the guinea-pig cochlea while monitoring various cochlear potentials. The drug (0.6-10 mM) had no effect on the magnitude of the compound action potential of the cochlear nerve, N1 latency, cochlear microphonics, or the summating potential (SP). The results are consistent with the hypothesis that the APB receptor is not involved in neurotransmission between cochlear hair cells and afferent nerve fibers.

Action Potentials↗
PubMedDate not supplied

Trimethyltin disrupts loudness recruitment and auditory threshold sensitivity in guinea pigs.

Trimethyltin (TMT) impairs auditory thresholds within minutes of systemic administration. However, there are no data which relate to the output of the auditory nerve at sound levels above threshold. In this experiment, we evaluated the functional effects of TMT on the auditory threshold by identifying the sound level which just produced a detectable compound action potential (CAP). We also assessed outer hair cell function by measuring the cochlear microphonic (CM), a nonpropagated ac potential which is phase-locked to the stimulus. Finally, we measured the growth of the N1 amplitude as a function of stimulus intensity at levels above threshold and of the summating potential (SP), a dc potential which has multiple generators. To isolate cochlear from systemic effects of TMT, the agent was applied directly to the round window, a structure separating the middle and inner ear, of anaesthetized guinea pigs. We show that TMT applied to the round window membrane can disrupt the function of the cochlea. Measurements of auditory function at supra-threshold levels showed clearly that TMT reduced the amplitude of N1 while having no measurable effect on the SP. These findings indicate that TMT blocks the recruitment of neuronal elements by loud sound. This pattern of impairment differs from that observed with aminoglycoside antibiotics, hypothermia, and presbycusis in which loudness recruitment has been reported.

Action Potentials↗