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R Thalmann

Publications and source records attributed to R Thalmann.

At least 55 records · Page 3Linked to original sources
PubMed1987

Dependence of endocochlear potential on vascular pH.

The vasculature of the inner ear was perfused with simple salt solutions which were buffered with HCO3/CO2, PO4 or Hepes (N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid). Replacement of HCO3/CO2 with either PO4 or Hepes at constant pH led to a rapid decline of about 15 mV in the endocochlear potential (EP) to a new steady-state level which could be maintained for over 30 min. This effect was reversible. Changes in [HCO3] over a wide range (nominally 0-100 mM) at constant CO2 tension produced only small (less than 3 mV) changes in the EP. However, the EP declined markedly when [HCO3] was maintained constant at 25 mM while CO2 tension was lowered. The response to increased CO2 was more complex. Additional experiments were performed in which intracellular pH was presumably altered by vascular perfusion of NH4 (alkalinization), or propionate (acidification). Perfusion of ammonium led to a strong decline of the EP (-38.2 +/- 2.5 S.D.) while propionate produced a small positive shift of about 3-4 mV. Acetazolamide (1 mM) decreased the EP by 7.6 +/- 2.7 mV and 14.8 +/- 4.6 mV in HCO3/CO2 and Hepes medium, respectively, after 10 min perfusion; this effect was poorly reversible. These results suggest that intracellular pH has a strong influence on the level of EP and further demonstrate that vascular [HCO3] and pH are not critical parameters for generation of the EP.

Acetazolamide↗
PubMed1987

Effect of iodoacetic acid upon cochlear potentials.

Lotz et al. reported that perilymphatic application of 5 X 10(-3) M iodoacetic acid (IAA) in the guinea pig does not influence the first-order cochlear microphonics (CM1) under aerobic conditions. However, in ischemia the rate of decline of the second-order microphonics (CM II, also called postmortem CM) was significantly increased by IAA. The authors concluded that glycolysis plays no role in maintaining the CMI, but that it is responsible for supporting the CMII. In carefully controlled experiments we found that in the respiring guinea pig, perilymphatic application of 5 X 10(-3) M IAA produced a rapid and pronounced effect upon both the endolymphatic potential and the CM. In particular, the CM dropped to less than 0.5% of its initial level within 40 min, due to IAA, whereas it took 120 min to drop to the same level in total ischemia (without IAA). We therefore reject the above-mentioned proposition that IAA is ineffective upon cochlear potentials under aerobic conditions; moreover, we find that even under aerobic conditions, the CM drops well below the usual CM II level substantially faster than under anaerobic conditions (without IAA). Other important findings, including an anoxia-sensitive negative component of the endolymphatic potential due to severe intoxication with IAA, and the effects of pretreatment of the organ of Corti with low concentrations of IAA upon the CM II are discussed.

Aerobiosis↗
PubMed1987

Mechanisms of endocochlear potential generation by stria vascularis.

It is commonly accepted that the endocochlear potential (EP) of the cochlea is generated by an electrogenic transport of potassium into scala media by the marginal cells of stria vascularis. We have studied the potential and potassium concentration gradients as stria vascularis was penetrated with double-barreled potassium selective electrodes in the guinea pig cochlea. Our data demonstrate that a region exists in stria which is positively polarized (higher than the EP), but which has a low (perilymph-like) potassium composition. It is concluded that EP cannot be generated by the marginal cells alone but may involve passive potassium movement across the apical membranes of the basal cells. A model is presented which is consistent with many anatomical and physiological features of stria vascularis.

Animals↗
PubMed1987

Composition and supramolecular organization of the tectorial membrane.

We have shown that collagen accounts for approximately 40% of the total protein of the tectorial membrane (TM) of the guinea pig and have estimated several essential parameters of TM composition including dry weight, wet weight, and water content. The major collagenous protein was definitively identified as type II collagen by SDS-PAGE, CNBr peptide mapping, and immunoblot assays. Quick-freeze, deep-etch electron microscopy of the guinea pig TM demonstrated a dense meshwork of fibers embedded in a complex microfibrillar matrix which may consist of proteoglycans; the larger fibers were similar in size and appearance to type II collagen fibers of elastic cartilage. Finally, the comparative free amino acid profiles of TM strongly suggest that the TM is chemically transparent with respect to endolymph. Thus, the TM appears to consist of a highly hydrated matrix mechanically stabilized by type II collagen fibers.

Amino Acids↗
PubMed1986

Direct measurement of longitudinal endolymph flow rate in the guinea pig cochlea.

The rate of longitudinal endolymph flow in the guinea pig cochlea has been measured with a novel tracer technique. The tracer we utilized was the tetramethylammonium (TMA) ion, the movement of which was monitored by ion-sensitive microelectrodes. Extremely small amounts of tracer were required as the electrodes could readily detect TMA concentrations in endolymph as low as 10 microM. TMA was introduced into scala media in the form of a small bolus, varying from 2-20 nl in volume. To examine whether longitudinal flow affects the dispersion of TMA in endolymph, we compared the characteristics of TMA spread to turn I following injection into turn II, with those of TMA spread to turn II following injection into turn I. The comparison of these data with an analytical model combining the processes of diffusion and volume flow demonstrates that the spread of tracer is dominated by passive diffusion processes with very little contribution from longitudinal endolymph flow. The rate of longitudinal endolymph flow between turn I and turn II was estimated to be less than 0.01 mm/min directed towards the basal turn. This value is considerably lower than recently published estimates using other techniques.

Cochlea↗
PubMed1986

Collagen--the predominant protein of the tectorial membrane.

Evidence is presented that, in contrast to the traditional view, a large proportion of the proteins of the tectorial membrane (TM) consists of collagen, primarily type II: characteristic amino acid composition of TM, including high levels of glycine, hydroxyproline and hydroxylysine; comigration of the main TM protein with appropriate collagen standards in two-dimensional gel electrophoresis; digestion of the main TM protein band following treatment with bacterial collagenase; one- and two-dimensional peptide mapping of cyanogen bromide digests of the TM exhibits patterns characteristic for collagen type II.

Amino Acids↗
PubMed1985

Effects of barium and ion substitutions in artificial blood on endocochlear potential.

Previously, a qualitative assessment was made (Marcus, D.C. (1984): Am. J. Physiol. 247, C240-C246) of the ion-selective properties of the cells bounding the cochlear duct by observing the effects of ion substitutions in the perilymph on the transepithelial potential difference (endocochlear potential; EP). Contributions by the marginal cells of the stria vascularis to the observed changes in the EP may have been masked, however, due to their 'isolation' from the perilymph by a continuous layer of basal cells. Since the ionic milieu of the basolateral membranes of the marginal cells is controlled more directly by the blood supply than by the perilymph, we report here on the effects of ion substitutions via vascular perfusion. Elevated K (substituted for Na or N-methyl-D-glucamine; NMDG) or Ba caused marked depression of the EP. Decreased Na or Cl (replaced by NMDG and gluconate, respectively) also depressed the EP. These changes in the EP were distinctly different from those observed previously by perilymphatic perfusion, and were interpreted in terms of a modified model of the strial marginal cells.

Barium↗
PubMed1985

Potassium-induced release of endogenous amino acids in the guinea pig cochlea.

Guinea pig cochleae were perfused with high-potassium solutions to depolarize hair cells artificially and induce the release of afferent neurotransmitter. Sequential injections of artificial perilymph containing 5 mM KCl, then 50 mM KCl, and finally 5 mM KCl were made into the scala tympani. This injection sequence was conducted under either normal divalent-cation conditions (2.0 mM CaCl2, 1.0 mM MgCl2) or calcium-deficient conditions intended to antagonize evoked transmitter release (0.1 mM CaCl2, 20.0 mM MgCl2). The levels of 21 endogenous primary amines in effluent collected from the scala vestibuli were determined by gradient-elution, reverse-phase HPLC using o-phthaldialdehyde-thiol adducts with fluorescence detection. Analyses indicated effluent concentrations of glutamate, taurine, and a coeluting taurine-gamma-aminobutyrate (GABA) fraction (but not GABA alone) increased significantly after exposure to 50 mM KC1 and returned to baseline levels after reintroduction of 5 mM KC1 under normal divalent-cation conditions. Correspondent changes in the release of these constituents were significantly attenuated under calcium-deficient conditions. This was not the case for potassium-induced changes in the release of arginine, aspartate, and isoleucine. These data are consistent with the hypothesis that the receptoneuronal transmitter is glutamate and further suggest a calcium-dependent mechanism involving taurine.

Amino Acids↗
PubMed1984

Prolonged maintenance of endocochlear potential by vascular perfusion with media devoid of oxygen carriers.

A method is described for maintaining the cochlear potentials of the guinea pig via arterial perfusion of the surviving inner ear with an artificial medium devoid of oxygen carriers or oncotic agents. The endocochlear potential (EP) can be maintained at a normal level for periods in excess of 5 h; the responses of the EP to anoxia and to furosemide closely approximate those seen in the intact animal. This preparation may represent a simplified method for carrying out selected arterial perfusion experiments in the surviving inner ear.

Animals↗
PubMed1984

Support of cochlear metabolic and ion transport processes solely by perilymphatic perfusion.

Morphologic considerations would seem to suggest that the cochlear duct could not be maintained in a fully functional state in the absence of a blood supply. We found, however, that perilymphatic perfusion could be used as a substitute for the normal vascular circulation. The criteria used to determine cochlear function included (1) normal endocochlear potential, (2) normal net secretory flux of rubidium (as a tracer for K), and (3) normal levels of ATP in both the organ of Corti and the stria vascularis. All criteria were satisfied by our perfusion regimen.

Adenosine Triphosphate↗
PubMed1983

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.

Animals↗
PubMed1982

Adenine nucleotides of the organ of Corti under metabolic stress.

The purpose of the reported experiments was to measure the concentrations of adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) in the organ of Corti in order to arrive at estimates of three commonly used adenylate ratios. Under normal conditions the concentrations of ATP, ADP, and AMP amounted to 15.8, 3.9, and 0.53 mmoles/kg dry weight, respectively. Of the three substances, AMP is the most sensitive indicator of metabolic stress, since ischemia of 65 seconds leads to an increase of 155%. Under normal conditions the adenylate energy charge, the energy status, and the phosphorylation state amounted to 0.83, 4.1, and 2.5 gram wet weight/mumole, respectively. Within 10 minutes of ischemia the energy charge had declined by 26%, the energy status by 50%, and the phosphorylation state by 76%. The apparent equilibrium constant of adenylate kinase of the organ of Corti was found to be 0.55. The potential significance of these data and their relationship to the situation in the stria vascularis are discussed.

Adenosine Diphosphate↗
PubMed1982

Effect of substrate-free vascular perfusion upon cochlear potentials and glycogen of the stria vascularis.

The effect of vascular perfusion of the anterior inferior cerebellar artery with synthetic blood containing no metabolic substrates upon the endolymphatic potential (EP) and the cochlear microphonics (CM) was determined in the guinea pig. In substrate-free perfusion the potentials were maintained for an average of 84 min. Subsequently, the EP declined at an average rate of 1.4 mV/min until a new steady-state level was temporarily established when the potential had dropped to about 30 mV. The decline of the CM appeared to be accounted for largely by the decline of the EP. During substrate-free perfusion prior to the onset of the decline of the potentials, the level of strial glycogen remained unchanged; glycogen decreased significantly only after the potentials had started to decline. When substrate-free vascular perfusion was accompanied by simultaneous substrate-free perilymphatic perfusion, the potentials started to decline immediately. On the basis of these data, we conclude that strial glycogen plays no role in the prolonged maintenance of the EP during substrate-free perfusion; rather, the potential seems to be maintained by entry of glucose (and presumably other substrates) from perilymph into the stria vascularis.

Animals↗