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Biomedical subjects

K Kuba

Publications and source records attributed to K Kuba.

At least 109 records · Page 6Linked to original sources
PubMed1980

Inhibitory action of Ca2+ on spontaneous transmitter release at motor nerve terminals in a high K+ solution.

The inhibitory effect of a high external Ca2+ ([Ca2+]o) on spontaneous transmitter release in a high K+ solution (Gage and Quastel 1966; Birks et al. 1968) was studied at the frog neuromuscular junction, based on the hypothesis that an increased intracellular free Ca2+ ([Ca2+]i) in the nerve terminal plays a key role in the depression. Three procedures were employed to increase [Ca2+]i; increasing [Ca2+]o, application of caffeine and tetanic nerve stimulation. All of these procedures increased m.e.p.p. frequency in normal Ringer. However, as the basic m.e.p.p. frequency was increased by raising the external K+ concentration (7--15 mM), their facilitatory effects on m.e.p.p. frequency decreased, dissapeared and eventually reversed to depressant actions. Since a rise in the external K+ concentration would increase the steady state level of [Ca2+]i, it is suggested that when the [Ca2+]i is preset at a high level, manipulations so as to further increase [Ca2+]i depress spontaneous release of transmitter. Possible mechanisms for this inhibition was discussed in relation to a question whether or not the rate of spontaneous transmitter release is a monotonic function of [Ca2+]i.

Acetylcholine↗
PubMed1980

An enzymatic approach to lipoprotein quantification.

Lipoprotein cholesterol levels were determined without ultracentrifugation by using modified enzymatic methods for cholesterol, high-density-lipoprotein (HDL) cholesterol, and triglyceride and the formula, low-density-lipoprotein (LDL) cholesterol = total cholesterol-HDL cholesterol-triglycerides/5. The methods for cholesterol and triglyceride determinations were standardized for accuracy and precision by the Center for Disease Control's Lipid Standardization Laboratory, which monitored this laboratory for 16 months. The lipoprotein cholesterol values obtained correlated well with lipoprotein cholesterol values determined at the Minnesota Lipid Research Clinic Laboratory using ultracentrifugation. LDL cholesterol determined at the Minneapolis Veterans Administration Hospital Laboratories (Y axis) produced a curve with an intercept of 9.38 mg/dl, a slope of .977, standard error of the estimate (Sy.x) of 8.8 mg/dl, and a correlation coefficient (r) of .983 (n = 32). HDL cholesterol was Y = 0.998 X + .89 mg/dl, Sy.x = 1.6 mg/dl (r = .984, n = 53), and very-low-density-lipoprotein (VLDL) cholesterol was Y = 1.010 X -1.32 mg/dl, Sy.x = 1.3 mg/dl (r = .996, n = 54).

Cholesterol↗
PubMed1980

Release of calcium ions linked to the activation of potassium conductance in a caffeine-treated sympathetic neurone.

1. The mechanism of spontaneous and rhythmic hyperpolarizations which occur in bullfrog sympathetic ganglion cells under the effect of caffeine (2--10 mM) were further analysed. 2. Intracellular injection of EGTA blocked generation of caffeine hyperpolarizations (C-hyperpolarizations): this confirmed the previous conclusion (Kuba & Nishi, 1976) that these hyperpolarizations are caused by rhythmic increases in the K+ conductance (GK) of the membrane as a result of rises in free intracellular Ca2+. 3. The amplitude and duration of a C-hyperpolarization induced by an action potential was a function of the time since the previous one; the longer the interval, greater the area. 4. The relationship between the product of the amplitude and duration of a C-hyperpolarization and the preceding interval depended on external Ca2+; when this was low the relationship shifted, so as to indicate an involvement of a Ca2+ accumulating process in the generation mechanism of C-hyperpolarizations. 5. A rapid lowering of temperature triggered the generation of a C-hyperpolarization before appearance of a rhythmic one. There seemed to be no threshold temperature for the effect of such a cold shock; cooling from any temperature within a certain range (10--25 degrees C) by more than a few degrees was effective. 6. The rapid cooling effect was observed even in a Ca2+-free Mg2+ solution. 7. Dantrolene Na increased the interval between rhythmic C-hyperpolarizations or blocked them, but affected less those triggered by an action potential or cold shock. 8. Intracellular injection of Ca2+ triggered the generation of a C-hyperpolarization before the appearance of a rhythmic one. 9. The latency of the generation of an action potential-evoked C-hyperpolarization was dependent on the preceding interval; the shorter the interval, the longer the latency. There was a refractory period for induction of an action potential-induced C-hyperpolarization. 10. The interval between rhythmic C-hyperpolarizations was increased by a small or moderate membrane hyperpolarization (5--20 mV) and decreased by a larger hyperpolarization; the refractory period of an action potential-induced C-hyperpolarization was similarly increased and then decreased by progressive membrane hyperpolarization. 11. These results suggest that rhythmic increases in the GK under the effect of caffeine are due to oscillations of the intracellular Ca2+ concentration and that there may be Ca storage sites in the bullfrog sympathetic ganglion cell which are comparable to the sarcoplasmic reticulum in the skeletal muscle fibre.

Animals↗
PubMed1980

Inhibition of transmitter release in bullfrog sympathetic ganglia induced by gamma-aminobutyric acid.

1. Effects of gamma-aminobutyric acid (GABA) on the nicotinic synapses in bullfrog sympathetic ganglia were studied. 2. When GABA (100 microM--1 mM) was applied to the ganglion, the post-synaptic membrane depolarized slightly and transiently with a slight decrease in the membrane resistance. 3. GABA (5 microM--1 mM) decreased the amplitude of the fast excitatory post-synaptic potentials (fast e.p.s.p.) and its quantal content without a significant change in the quantal size, and these effects were seen even after the subsidence of the membrane depolarization. Picrotoxin (10 microM) did not antagonize the GABA action. 4. The sensitivity of the subsynaptic membrane to ACh was unaffected by GABA. On the other hand, the synaptic current underlying the fast e.p.s.p. was significantly depressed in the presence of GABA. 5. Neither the frequency nor the amplitude of the miniature e.p.s.p.s which occurred spontaneously were altered by GABA, in either normal or high K+ solutions. 6. The depressant action of GABA on the fast e.p.s.p. was not changed in a high K+ solution, while it was markedly decreased in a Cl- -deficient solution. 7. A small, but significant reduction in the amplitude of the presynaptic terminal spike recorded with a focal extracellular electrode was observed under the effect of GABA. 8. It was concluded that GABA inhibits synaptic transmission of bullfrog sympathetic ganglion mainly by decreasing the evoked release of transmitter and only partly by post-synpatic action. Possible mechanisms of the presynaptic action of GABA were discussed.

Acetylcholine↗
PubMed1979

Characteristics of fast excitatory postsynaptic current in bullfrog sympathetic ganglion cells. Effects of membrane potential, temperature and Ca ions.

The membrane current underlying the fast excitatory postsynaptic potential (EPSC) of bullfrog sympathetic ganglion cells was studied. The relationship between the EPSC amplitude and membrane potential was linear at negative levels of membrane potential, but deviated from the linearity toward a smaller amplitude at positive levels. The falling phase of EPSC almost followed a single exponential decay. The half-decay time (HDT) of EPSC's increased exponentially with an increase in the negativity of membrane potential. The rise time (RT) was also prolonged slightly with membrane hyperpolarization. Lowering of temperature decreased the EPSC amplitude, lengthened markedly the HDT and increased the slope relating the logarithm of the HDT to membrane potential. Neostigmine (1 x 10(-5) M) prolonged both the RT and HDT. A decrease in Ca2+ concentration caused a marked reduction in the EPSC amplitude, and a slight shortening in the RT and HDT. An increase in Ca2+ concentration significantly prolonged the RT and HDT without altering the slope of the relationship between the HDT and membrane potential, while the amplitude of EPSC was increased slightly. The HDT was independent of EPSC amplitude. It is suggested that the mechanism responsible for closing the ion channels of the nicotinic receptor at the subsynaptic membrane is regulated by membrane potential. The possible mechanisms of the action of Ca2+ on the decay phase of EPSC were discussed.

Animals↗
PubMed1979

Four electrophoretic methods compared for diagnosis of type III hyperlipoproteinemia.

Blood drawn from 192 probands and 1129 first-degree relatives who were participants in a collaborative family study of hyperlipoproteinemia at nine Lipid Research Clinics was used to prepare aliquots of whole plasma and top (d less than 1.006 g/mL) and bottom (d greater than 1.006 g/mL) ultracentrifugal fractions. Each aliquot was analyzed at a central laboratory by electrophoresis on paper, agarose, and polyacrylamide gel, and by a combined electrophoretic precipitation technique. The electrophoretograms were evaluated for the presence or absence of a "floating-beta" lipoprotein band. All four methods agreed completely for 92.3% of the samples. An additional 2.0% of the samples were in agreement for three electrophoretic methods, but the paper electrophoretic results were not interpretable. Another 1.9% were considered to be "floating-beta" positive by paper electrophoresis but negative by the other three electrophoretic methods.

Chemical Precipitation↗
PubMed1978

An enzymatic triglyceride method that is suitable for long-term population studies.

An enzymatic triglyceride method has been shown to be a suitable alternative to the Lipid Research Clinics' extraction/fluorometry method in long-term population studies. Correlation of results obtained with this method by this laboratory (y-axis) and by the Minneapolis Lipid Research Clinic Laboratory (x-axis) during a nine-week standardization period produced a curve with an intercept of -72 mg/liter, a slope of 1.019, and a correlation coefficient of r=0.996 (n=47). During this standardization period certain methodological problems were observed and corrected. An increase in background in certain clinical specimens, caused by spontaneous degradation of NADH, was observed, accurately measured, and taken into account when appropriate.

Glycerol Kinase↗
PubMed1978

Multi-laboratory comparison of three heparin-Mn2+ precipitation procedures for estimating cholesterol in high-density lipoprotein.

Plasma high-density lipoprotein is commonly estimated by measuring the cholesterol remaining in plasma supernatant solutions after other lipoproteins, which contain apolipoprotein B, are precipitated with heparin and Mn2+. The method (method I) now in use by the Lipid Research Clinics, in which Mn2+ is at 46 mmol/liter final concentration, is reasonably accurate, but precipitation and sedimentation of lipoproteins other than high-density lipoproteins is often incomplete. We evaluated two modifications of method I. In method II, the Mn2+ concentration was doubled; the second modification (method III) included the increased Mn2+ concentration in a combined heparin Mn2+ reagent, decreased sample volume (2 ml), and a shorter incubation time (10 min at room temperature). The percentages of samples with turbid supernates (i.e., incomplete sedimentation) by methods I, II, and III were 9, 3, and 2%, respectively. Among non-turbid supernates, the percentages of samples containing measurable apolipoprotein B (incomplete precipitation) were 79, 19, and 16%, respectively. We conclude that method III is the most convenient and accurate of the three procedures.

Chemical Precipitation↗
PubMed1977

Polygraphic study on the clinical seizures induced during nocturnal sleep.

The subjects of this study consisted of 17 epileptic patients with clinical seizures during all-night sleep recording (the seizure group) and another 17 epileptic patients without clinical seizures (the control group). The results obtained were as follows: 1) The 50-90% out of total clinical seizures were induced in non-REM sleep, while a few clinical seizures were induced in REM sleep. The number of clinical seizures in sleep stage of higher activity level increased as the incidence of clinical seizure during all-night grew. 2) In the seizure group REM sleep could not be detectable during all-night in five cases out of 17 cases, while we could not find cases lacking REM sleep in the control group. This difference between two subject groups was statistically significant (P less than 0.025). 3) As to focal spike group, the spike discharge incidence of total sleeping time and of each sleep stage was higher respectively in the seizure group than that in the control group, and particularly in St.1, St.2 and REM sleep the figure of the discharge incidence was found significantly higher in the seizure group than that in the control group (P less than 0.05). We discussed on above-mentioned results, and we emphasized particularly that REM-sleep suppresses clinical seizures, although non-REM sleep induces clinical seizures.

Adolescent↗