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Biomedical subjects

C Bergman

Publications and source records attributed to C Bergman.

At least 37 records · Page 2Linked to original sources
PubMed1992

MR angiography in children with cerebral neurovascular diseases: findings in 31 cases.

OBJECTIVE: We evaluated the suitability of MR angiography for routine use in children with suspected intracranial vascular disease. SUBJECTS AND METHODS: Thirty-one children, 6 months to 14 years old, with intracranial lesions or clinically suspected vascular malformations were studied prospectively with conventional MR imaging and time-of-flight MR angiography. In nine cases, MR angiographic findings were verified with digital subtraction angiography or conventional angiography. All MR studies were performed on a 1.5-T MR system using a circularly polarized head coil. RESULTS: Arterial MR angiography, performed in 24 cases, revealed congenital abnormalities of the arterial vessels in 20 cases. Vessel stenosis was observed in nine patients, and displacement of intracranial arteries due to tumors could be seen in 10 patients. Seven children had no abnormal findings. Venous MR angiography was performed in seven children, with depiction of sinus thrombosis in six cases. The comparative analysis of MR angiography and digital subtraction angiography showed equivalent results in nine patients; in one patient the degree of stenosis was overestimated with MR angiography. CONCLUSION: MR angiography, when combined with MR imaging, reveals information about soft-tissue and vascular structures in a single setting. At this point, MR angiography can replace invasive conventional angiography or digital subtraction angiography only in selected cases because of software and hardware limitations. Arterial or venous MR angiography can be helpful as an additional scan in MR examinations of children with suspected cerebral neurovascular diseases, and its noninvasive nature makes it well suited for routine use in children.

Adolescent↗
PubMed1991

A possible Na/Ca exchange in the follicle cells of Xenopus oocyte.

In manually dissected Xenopus oocytes, we found that the replacement of external sodium by Tris, choline, or lithium induced a large membrane depolarization and, in voltage clamp, a large inward current. This current appears to be due to activation of a calcium-dependent chloride conductance since it is reversed near ECl, increased by the removal of external chloride, and can be abolished by an injection of BAPTA or by the removal of external Ca2+. Using the Ca-dependent Cl current as a monitor of Ca concentration at the inner surface of the oocyte membrane, we are led to propose that the removal of external Na+ induces an increase in internal Ca2+ via the activation of a Na/Ca exchanger operating in the reverse mode. This interpretation is supported by the finding that the chloride current is diminished in either 3',4'-dichlorobenzamyl (DCB) or high external [Mg2+]o, both of which are known to block the Na/Ca exchanger, whereas it is increased when Li+, rather than Tris or choline, is used as the substitute for Na. The effect of zero [Na+]o was not obtained in oocytes from which follicular cells were removed by enzymatic treatment. This observation led us to test the possibility that the Na/Ca exchanger was present in the follicle cells and not in the oocyte membrane, assuming that entering Ca2+ could pass into the oocyte through gap junctions. Octanol, which blocks gap junctions, or a high [Ca2+]o both considerably reduced the inward current. While octanol probably blocked the gap junctions directly, we propose that the block by high [Ca2+] was due to an excessive rise of [Ca2+]i in the follicular cells. These results, taken together, indirectly suggest the presence of a Na/Ca exchanger in the follicular cells. These results, taken together, indirectly suggest the presence of a Na/Ca exchanger in the follicle cells of Xenopus oocyte which could contribute to the regulation of the internal Ca concentration of the oocyte before fertilization.

Amiloride↗
PubMed1989

Electrophysiological investigation of the amino acid carrier selectivity in epithelial cells from Xenopus embryo.

The electrical responses induced by external applications of neutral amino acids were used to determine whether different carriers are expressed in the membrane of embryonic epithelial cells of Xenopus laevis. Competition experiments were performed under voltage-clamp conditions at constant membrane potential. Gly, L-Ala, L-Pro, L-Ser, L-Asn and L-Gln generate electrical responses with similar apparent kinetic constants and compete for the same carrier.They are [Na]o and voltage-dependent, insensitive to variations in [Cl]o and [HCO3]o, inhibited by pHo changes, by amiloride and, for a large fraction of the current, by MeAIB. The increase in [K]o at constant and negative membrane potential reduces the response, whereas lowering [K]o augments it. L-Leu, L-Phe and L-Pro appear to compete for another carrier. They generate electrogenic responses insensitive to amiloride and MeAIB, as well as to alterations of membrane potential, [Na]o and [K]o. Lowering [Cl]o decreases their size, whereas increasing [HCO3]o at neutral pHo increases it. It is concluded that at least two and possibly three transport systems (A, ASC and L) are expressed in the membrane of the embryonic cells studied. An unexpected electrogenic character of the L system is revealed by the present study and seems to be indirectly linked to the transport function. L-Pro seems to be transported by system A or ASC in the presence of Na and by system L in the absence of Na. MeAIB induces an inward current.

Amino Acid Transport Systems↗
PubMed1985

Origin and voltage dependence of asparagine-induced depolarization in intestinal cells of Xenopus embryo.

The kinetics and voltage dependence of asparagine (Asn)-induced depolarization in endoderm cells from Xenopus laevis embryos were analysed using current-clamp techniques. The depolarization is assumed to reflect the activation of an amino acid membrane carrier; it is accompanied by a slight increase in membrane resistance and cannot be explained by only the electrogenic character of the Asn carrier. It is proposed that the Asn depolarization arises, at least in part, from the decrease of the permeability ratio PK/PNa indirectly associated with the Na-coupled amino acid uptake. At room temperature (20-23 degrees C) the Asn response develops according to a single exponential function whose time constant is correlated with the final level of depolarization. Both amplitude and rise time of the depolarization are sensitive to variations of membrane potential and changes in Asn or Na external concentrations. Lowering the temperature decreases the amplitude of the Asn depolarization and increases its rise time with a Q10 factor of two; the kinetics remain of the Michaelis-Menten type, with a marked decrease in delta Emax and no change in Km. When the holding potential is altered by depolarizing and hyperpolarizing currents, the Asn response varies according to a bell-shaped characteristic presenting an optimum near the normal resting level. Membrane depolarizations induced by Na/K-pump inhibitors or high external K concentrations reduce the size of the Asn response; repolarizing the cell by current injection does not reverse the inhibitory effect of external K ions. Hyperpolarizing the membrane with a K-free Ringer solution increases the amplitude of the Asn response. In all these cases a decrease in delta Emax accounts for the apparent voltage sensitivity of the carrier mechanism. When induced by alterations of [K]o, an additional change in Km is observed, suggesting a K/Na-competitive inhibition of the Asn carrier. The results are discussed in terms of the amino acid carrier and passive membrane properties. It is suggested that the outward K-electrochemical gradient contributes an additional source of energy to the Na-dependent Asn uptake.

Animals↗
PubMed1981

Electrogenic responses induced by neutral amino acids in endoderm cells from Xenopus embryo.

1. Membrane potential measurements were carried out on endoderm cells from early Xenopus embryos in order to study neutral amino acid transport in non-excitable cells. 2. The electrical properties of the cell membrane were studied under normal conditions, then in the presence of various Na/K-pump inhibitors and at different Na, K and Cl concentrations in Ringer solution. Blockade of the Na/K-pump by ouabain, Li, cooling to 10 degrees C or low [Na]0 induces similar depolarizations of about 40 mV. 3. External application of various neutral L-amino acids induces reversible membrane depolarizations. The D-isomeric forms are found to be ineffective. The amino acid induced depolarizations are not accompanied by changes in membrane resistance. They do not show voltage dependence for potential changes of less than 40 mV. 4. The amino acid depolarization increases with increasing concentration and follows first order Michaëlian kinetics. Both the size and the time course of the amino acid depolarization depend on [Na]0. Increasing [Na]0 markedly increases the apparent affinity of the membrane receptor for amino acid. 5. Increasing [k]0 reduces the size of the amino acid response. Short exposures to either ouabain or Li do not alter the amino acid depolarization. However, p time course of the amino acid depolarization depend on [Na]0. Increasing [Na]0 markedly increases the apparent affinity of the membrane receptor for amino acid. 5. Increasing [k]0 reduces the size of the amino acid response. Short exposures to either ouabain or Li do not alter the amino acid depolarization. However, p time course of the amino acid depolarization depend on [Na]0. Increasing [Na]0 markedly increases the apparent affinity of the membrane receptor for amino acid. 5. Increasing [k]0 reduces the size of the amino acid response. Short exposures to either ouabain or Li do not alter the amino acid depolarization. However, prolonged exposure to pump inhibitors or marked alteration of the Na concentration gradient leads to a complete inhibition of amino acid responses. 6. The results are in good agreement with the notion that the amino acid induced responses reflect the activation of an electrogenic amino acid carrier, very likely co-transporting Na and amino acid.

Animals↗
PubMed1979

The action of salicylate ions on the frog node of Ranvier.

1. The effects of salicylate on the membrane currents in the frog node of Ranvier were investigated. 2. External salicylate slows the falling phase of the action potential, with little effect on the action potential amplitude. 3. External salicylate has no effect on the leak current. 4. Most of the actions of external salicylate can be attributed to a simple incorporation of negative charge into the membrane surface. The h infinity, tau h, tau m and m infinity curves for the sodium current are shifted to more negative potentials, as are the n infinity and k infinity curves for the potassium current. Potassium ion accumulation prevented analysis of the action of salicylate on the time constant of the potassium current kinetics. 5. In addition to the h infinity and tau h curves being shifted to more negative potentials, the shapes of the curves are also changed by salicylate. These shape changes cannot be explained by conventional homogeneous surface charge theory. Possible explanations for these changes are discussed. 6. Internal salicylate has similar effects to external salicylate: the gating variable curves for the sodium current are shifted in the negative direction on the voltage axis, rather than in the positive direction expected if negative charge were added to the inner surface of the nodal membrane. This may be due to salicylate crossing the membrane and binding preferentially to a receptor at the external surface, or might be due to a rise in intracellular calcium concentration following inhibition of oxidative phosphorylation.

Action Potentials↗
PubMed1976

Decreased rate of sodium conductance inactivation in the node of Ranvier induced by a polypeptide toxin from sea anemone.

The effects of two toxins extracted from the tentacles of Anemonia sulcata on ionic currents have been tested on the nodal membrane of myelinated nerve fibres from Rana esculenta. While external application of Toxin I at 100 muM leaves both specific ionic currents unmodified, Toxin II at 10 muM reacts with a receptor site associated with the sodium conductance inactivation gating. Since internal application by diffusion of Toxin II at a concentration of 700 muM leaves the ionic currents unchanged, the receptor site is most likely located on the external side of the nodal membrane. An equilibrium dissociation constant for the effects of Toxin II was estimated as 20 muM. The on-reaction is fast (rate constant for the on-reaction roughly equal to 3.103 M-1) suggesting a readily accesible receptor site for the toxin. The kinetics characteristics of the sodium currents recorded in the presence of Toxin II suggest that there are at least two steps in the reaction leading to Na+ -channels with the inactivation gate completely immobilized. The relatively fast reversibility of the intermediate stage of the reaction and the rather slow but, in the end, complete reversal of the toxin effects suggest that the toxin acts by modifying the energy profile for the transition "inactivation gate in the open configuration to inactivation gate in the closed configuration." Toxin II at higher concentrations (greater than 100 muM) also inhibits the potassium currents but these effects were not studied in any detail.

Animals↗
PubMed1976

[Inhibition of the sodium inactivation of the nodal membrane by anemonia sulcata toxin II].

A neurotoxin (ATX-II) extracted from the tentacles of Anemonia sulcata has been found to interact with the sodium channel of the nodal membrane in myelinated nerve fibres from Rana esculenta. If externally applied at low concentration (Kd = 20 muM), it reduces considerably the rate of inactivation of the sodium conductance without affecting the activation. At such concentrations, the potassium conductance is not affected. If internally applied ATX-II does not affect the membrane conductance.

Animals↗
PubMed1975

Potassium accumulation in the perinodal space of frog myelinated axons.

1. Voltage clamp experiments were carried out on frog myelinated fibres to study the origin of the transient inward current occuring when the membrane is repolarized after long lasting depolarizing pulses (tail current denominated "Ip" by Frankenhaeuser). 2. The "tail" of inward current measured during repolarization after break of the depolarizing pulse is insensitive to external application of TTX, is abolished by external treatment with TEA or Cs and decreases when the outward K-current during the pulse is diminished. 3. The time course of the "tail" current is exponential. Its direction depends on the duration of the depolarizing pulse and on the membrane potential level at repolarization. 4. It is concluded that the tail of inward current during repolarization is carried by K-ions accumulated in the perinodal space during a depolarizing pulse. The data suggest that the tail reflects the time course of the restoration of the K-concentration to its initial level. The tail current itself contributes to this restoration depending on the Em value at repolarization. 5. It is shown that one of the two phenomenological models proposed by Frankenhaeuser and Hodgkin to account for the external potassium accumulation observed in the squid giant axon may be also applied to the Ranvier node. Assuming that the thickness of the space is 2900 A and that the K-permeability of the barrier is 0.019 cm/sec, it is possible to account for the observed changes in [K]0 during a long lasting depolarizing pulse. 6. The existence of such a barrier would introduce an electrical resistance in series with the nodal membrane of roughly 150 000 omega.

Aniline Compounds↗
PubMed1975

Cesium induced rectifications in frog myelinated fibres.

Voltage clamp experiments done on nodes of Ranvier show that external application of Cesium blocks the inward but not the outward potassium currents. Internal application of Cs ions reduces the outward K-current and the inward K-current is not affected. These results support the hypotheses that K ions cross th- K-channel after dehydration at superficial sites where competition may occur with Cs-ions.

Animals↗
PubMed1975

Late sodium current in the node of Ranvier.

Voltage clamp experiments carried out on nodes of Ranvier of myelinated fibres of Rana esculenta showed that a small fractoon of sodium channels fail to inactivate. Thus during long lasting depolarizing pulses there is a small Na-current superimposed on the leakage and potassium currents. This late Na-current appears more marked in sensory fibres than in motor ones.

Animals↗