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At least 343 records · Page 19Linked to original sources
PubMed1999

Auditory collusion and a coupled couple of outer hair cells.

The discrepancies between measured frequency responses of the basilar membrane in the inner ear and the frequency tuning found in psychophysical experiments led to Bekesy's idea of lateral inhibition in the auditory nervous system. We now know that basilar membrane tuning can account for neural tuning, and that sharpening of the passive travelling wave depends on the mechanical activity of outer hair cells (OHCs)3, but the mechanism by which OHCs enhance tuning remains unclear. OHCs generate voltage-dependent length changes at acoustic rates, which deform the cochlear partition. Here we use an electrical correlate of OHC mechanical activity, the motility-related gating current, to investigate mechano-electrical interactions among adjacent OHCs. We show that the motility caused by voltage stimulation of one cell in a group evokes gating currents in adjacent OHCs. The resulting polarization in adjacent cells is opposite to that within the stimulated cell, which may be indicative of lateral inhibition. Also such interactions promote distortion and suppression in the electrical and, consequently, the mechanical activity of OHCs. Lateral interactions may provide a basis for enhanced frequency selectivity in the basilar membrane of mammals.

Animals↗
PubMed1998

Gadolinium determination in tissue samples by inductively coupled plasma mass spectrometry and inductively coupled plasma atomic emission spectrometry in evaluation of the action of magnetic resonance imaging contrast agents.

The quantitative determination of Gd-containing magnetic resonance imaging (MRI) contrast agents in animal tissues is performed by both ICP-AES and ICP-MS. While ICP-AES has been used to determine Gd-containing contrast agents by other workers, no published methodology has been found. An accurate and precise method using nitric acid and microwave digestion for sample preparation is described. Dosed rat tissue, blood and plasma were measured by both ICP-AES and ICP-MS. The ICP-AES method is excellent for screening Gd levels and quantitative determination of concentrations above 400 ng ml-1, but it lacks the sensitivity to measure agent concentrations in low dose MRI studies. This work demonstrates that ICP-MS has the needed sensitivity to replace radiotracer methods currently used for low dose studies, while maintaining the accuracy and precision of results obtained by ICP-AES. Gadolinium detection limits in tissue were 0.04 mumol of Gd per kg of tissue, an order of magnitude lower than studies using radiotracer techniques.

Animals↗
PubMed1996

Activation of phosphatidylinositol 3-kinase by concanavalin A through dual signaling pathways, G-protein-coupled and phosphotyrosine-related, and an essential role of the G-protein-coupled signals for the lectin-induced respiratory burst in human monocytic THP-1 cells.

Stimulation of monocytic THP-1 cells by a lectin, concanavalin A (Con A), resulted in protein-tyrosine phosphorylation and association of some of the thus phosphorylated proteins with the 85 kDa regulatory subunit of PtdIns 3-kinase. Both actions of Con A were not inhibited by wortmannin, a PtdIns 3-kinase inhibitor, or by prior exposure of cells to pertussis toxin which uncouples certain G-proteins from receptors. The binding of PtdIns 3-kinase to the tyrosine-phosphorylated proteins increased upon Con A stimulation; there was a marked increase in the enzymic activity in the anti-phosphotyrosine immuno-precipitates from Con A-treated cells. The increase was abolished by wortmannin but not affected by pertussis toxin. The incorporation of 32P into PtdInsP3 also increased during incubation of [32P]P(i)-prelabelled cells with Con A, reflecting activation of whole-cell PtdIns 3-kinase which could not be accounted for solely by the increase in the phosphotyrosine-bound enzyme activity from the following aspects: (1) different concentration dependencies for Con A; and (2) almost total susceptibility of the incorporation to pertussis toxin. This notion appears to be supported by different time courses between increases in PtdInsP3 production and the phosphotyrosine-bound activity. The susceptibility to the toxin may reflect involvement of the toxin-sensitive G-proteins. In contrast, insulin-induced increases in PtdInsP3 production, as well as increases in phosphotyrosine-bound PtdIns 3-kinase activity, were blocked by wortmannin, but never affected by prior exposure of cells to pertussis toxin, excluding a possible involvement of G-proteins in the insulin-induced activation. Con-A-induced O2- production was almost inhibited by either pertussis toxin or wortmannin. These results suggest that oligomerization of cell-surface glycoproteins with Con A gives rise to activation of G-protein(s) and certain tyrosine kinase(s), both of which were responsible for PtdIns 3-kinase activation; the G-protein-mediated activation led to the respiratory burst.

Amino Acid Sequence↗
PubMed1993

Functional study on the effects of nifedipine, cromakalim, and the absence of extracellular Ca2+ on alpha 1-adrenoceptor-mediated excitation-contraction coupling in isolated rat portal vein: comparison with depolarization-mediated excitation-contraction coupling.

The effects of Ca(2+)-entry blockade by nifedipine, K+ channel opening by cromakalim, and of omitting extracellular Ca2+ on the contractile response elicited by a supramaximum concentration of the "full" and selective alpha 1-adrenoceptor agonist phenylephrine (10(-4) M) were compared with those elicited by a supramaximal concentration of KCl (50 mM) in isolated rat portal vein. The contractile response to phenylephrine appeared to be biphasically composed of an early "transient" phase and a slowly developing "sustained" phase that reached maximum values after 30 s and 5 min after initiation of contraction, respectively. The contractile response to KCl (50 mM) exhibited a triphasic pattern consisting of "spike," "transient", and "sustained" components that peaked after 8 s, 25 s, and 10 min, respectively. Nifedipine was able to eliminate all components of the contractions in response to both phenylephrine and KCl almost completely. Nifedipine was approximately 10 times more potent at suppressing the slowly developing sustained components of the contractions in response to both stimuli than the early transient components. The spontaneous myogenic contractions were inhibited by nifedipine with intermediate potency. Cromakalim, in contrast to nifedipine, selectively eliminated the early transient components of the contractions in response to both phenylephrine and KCl. The sustained components of the contractions in response to both stimuli were relatively resistant to K+ channel opening, although higher concentrations (> 1 microM) of cromakalim were capable of antagonizing the sustained response to phenylephrine accompanied by oscillations in tone. Cromakalim was most potent in counteracting spontaneous myogenic contractions. When phenylephrine and KCl were added with or without external Ca2+ after different periods of equilibration in nominally Ca(2+)-free medium, different washout kinetics for the different components of the contractions in response to both stimuli were observed. The early transient phases of tension development in response to both stimuli were completely lost after approximately 6 min of equilibration in nominally Ca(2+)-free medium, whereas the slowly developing sustained components of the contractions were immediately lost after the change to nominally Ca(2+)-free medium. Externally added Ca2+, when administered together with phenylephrine or KCl after the preparations had been exposed for different times to nominally Ca(2+)-free medium, could not restore the early transient components.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗