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T Brismar

Publications and source records attributed to T Brismar.

At least 19 recordsLinked to original sources
PubMed1992

Nerve conduction in the hands of vibration exposed workers.

Symptoms of peripheral neuropathy in the hands are common among workers using vibrating tools. The mechanism for this and its relation to carpal tunnel syndrome (CTS) was studied in workers exposed to vibration at their workplace (17), along with a control group of healthy construction workers with heavy manual work but without vibration exposure (10). Patients with uni- or bilateral CTS (11) and a group of healthy volunteers without manual work (9) were included for comparison. Median nerve conduction velocities were measured both over the carpal tunnel and in a more distal segment. Vibration exposed workers had similar conduction velocities to unexposed construction workers. The subgroup of vibration exposed patients with symptoms from the hands had normal conduction in the ulnar nerve but demonstrated a decrease in median nerve conduction comparable (but less pronounced) with the CTS group. On a group basis these results indicated that the median nerve is most vulnerable for hand-arm vibrations. However, the conduction defects were not pronounced enough to diagnose CTS in most individual cases.

Adult↗
PubMed1991

Mechanism of anoxic conduction block in mammalian nerve.

The mechanism by which anoxia blocks impulse conduction was studied in isolated sciatic nerves from the rat. The desheathed nerve was mounted in a recording chamber, and the compound action potential (CAP) was measured at controlled temperature (23 and 37 degrees C). When the nerve was irrigated with nitrogenated Ringer's solution compound action potential decreased to 50% in 10 min at 37 degrees C and in 35 min at 23 degrees C, whereas in oxygenated solution compound action potential decreased less than 5% in 60 min. A Na-free nitrogenated solution similarly caused anoxic block, that is the effect was independent of impulse activity. Ouabain (1 mM) decreased compound action potential by only ca. 4% in 30 min, and the effect of anoxia was delayed in presence of ouabain. Dinitrophenol (0.05 mM) reduced compound action potential to 50% in 5 min. These findings indicated that the anoxic block was not related to changes in axonal concentration of Na or K following impulse activity or inhibition of Na-K-ATPase. Instead the findings imply that the anoxic block is due to inactivation of Na-channels as a consequence of inhibition of another ATP-dependent process in the axon.

Action Potentials↗
PubMed1991

In vivo analysis of intracellular thallium-201 accumulation in skeletal muscle of the rat.

The specific accumulation of the K(+)-analogue Tl+ (201Tl+) in muscle after intramuscular injection was analysed by gamma spectrometry in vivo of rat hamstring muscles. A mixture (0.1 ml) of 201Tl+ (thallous+ chloride-) and 99mTc-pertechnetate- (Na+ pertechnetate-) was given, by which 99mTc-pertechnetate- served as a reference substance with negligible intracellular accumulation. After 30 min 8.9 +/- 5.8% of injected 99mTc-pertechnetate- remained in the muscle and 49 +/- 10% of 201Tl+ (+/- SD, n = 18). The difference between 201Tl+ and 99mTc-pertechnetate- at 30 min was taken as a measure of the intracellular 201Tl+ accumulation, which was 40% of the initial amount of 201Tl+. The half-time of the calculated intracellular 201Tl+ accumulation was 4.9 +/- 1.9 min. In the presence of ouabain (1.0 mM in the injectate) the intracellular 201Tl+ accumulation was 25 +/- 10% (n = 7), that is ouabain decreased the intracellular 201Tl+ accumulation by 38% (P = 0.0035). Non-radioactive Tl+ (1.0 mM Tl-acetate in the injectate) inhibited the uptake by 35% (P = 0.0013). Ouabain did not significantly affect the half-time for the Tl+ uptake. An increase in [K+] of the injectate from 0 to 5 mM had no significant effect. Insulin (0.2 units in the injectate) had no effect. It is concluded that the specific Tl(+)-accumulating properties of muscle fibres can be studied with the present in vivo technique, which can provide information about the Na-K-ATPase activity and the membrane potential of muscle fibres.

Animals↗
PubMed1990

Hearing loss from the acoustic artifact of the coil used in extracranial magnetic stimulation.

The stimulating coil used in extracranial magnetic field stimulation (EMFS) emits a high intensity impulse sound artifact that causes permanent threshold shifts in the unprotected ears of experimental animals. At magnetic stimulation levels of 50 to 100%, the magnetic coil acoustic artifact (MCAA) ranged from 145 to 157 dB peak sound pressure level at the eardrum. The magnetic field alone did not appear to cause hearing impairment since no threshold shifts were observed in ears that were plugged with ear protectors during exposure to the MCAA. These findings suggest that the acoustic artifact produced by EMFS in the clinic may pose some risk for hearing loss in patients and clinicians when held in close proximity to the unprotected ear. We recommend the use of ear protectors for the patient and clinician during EMFS as a precautionary measure to prevent hearing loss.

Animals↗
PubMed1989

Thallium-201 uptake relates to membrane potential and potassium permeability in human glioma cells.

The mechanism for 201Tl+ uptake was studied in cultured human glioma cell lines. Ouabain (1 mM) decreased the uptake at steady-state to 60%, but the rate of uptake was faster in the presence of ouabain. Addition of non-radioactive Tl+ (to a K+-free medium) decreased the uptake, but much less than expected for a system limited by the number of transport sites. Changes in K+ concentration of incubation medium affected the 201Tl+ uptake as predicted by the electrochemical equilibrium (Nernst equation). Using the uptake in isotonic KCl as a reference for membrane potential (0 mV), the calculated membrane potential was -75 mV in a medium with 3.0 mM K+. The Tl+-flux constants and the membrane permeabilities for Tl+ and K+ were calculated from the rate of uptake and from wash-out experiments. This is a new method for membrane potential and permeability studies in cell populations. The mechanism for 201Tl+ uptake is relevant for the clinical interpretation of 201Tl+ scintigraphy.

Humans↗
PubMed1989

[Cellular mechanisms in diabetic neuropathy].

Although the pathogenesis of distal diabetic neuropathy is still uncertain, a possible mechanism might be postulated on the basis of results of several experimental studies. Differences between animal and human models are obvious--especially with regard to the time factor, but in attempts at elucidating basic mechanisms use can be made of the close resemblance between animal and human nerve fibres at the cellular and molecular level. A decrease in sodium potassium ATPase activity, causing intracellular accumulation of oxidised sodium, cellular oedema, and myelin detachment around the nodes of Ranvier, would seem to be the central component in the pathogenesis.

Adenosine Triphosphatases↗
PubMed1989

Inward rectifying potassium channels in human malignant glioma cells.

Human glioma cells obtained from established cell lines (Tp-276MG, Tp-301MG, Tp-378MG, Tp-483MG and U-251MG) were analyzed for the presence of ion channels with the tight-seal voltage clamp technique. The current-voltage relation revealed a marked inward rectification at hyperpolarizing voltages, due to the presence of inward rectifying K-channels in cells from all studied cell lines. These channels were conducting when the membrane potential was more negative than the K-equilibrium potential. The slope conductance for the inward K-currents (gKi) was affected both by [K+]i and [K+]o. gKi was proportional to [K+]o raised to 0.35 or 0.50, of which the larger value was measured in the presence of low [K+]i (25 mM). The rectification was not significantly different in cells perfused with Mg-free EDTA-buffered internal solution. Tl+ was 3.5 times more permanent than K+. gKi was blocked by Cs+ (1 mM) in a voltage-dependent way (more effective in the hyperpolarized membrane), and by Na+ (154 mM) depending on voltage and time. From measurements of unitary current events in membrane patches (outside out or cell attached) the conductance of the single inward rectifying channel was estimated to be 27 +/- 7 pS. This type of ion channel may be important for K-uptake by glial cells and hence for the K-homeostasis in the brain.

4-Aminopyridine↗
PubMed1989

Potassium and sodium channels in human malignant glioma cells.

Human malignant glioma cells from 5 different cell lines were voltage clamped and examined for the presence of depolarization-activated ion channels. Outward K-currents were elicited at membrane potentials greater than 40 mV, which had two main components, one which was delayed and blocked by externally applied tetraethylammonium (TEA, 10 mM), and another which was instantaneous and insensitive to TEA in the outside solution. The proportion of the two K-current components varied between cell lines. An increase in [Ca2+]o in the range 0-4 mM, decreased the leak conductance and shifted the activation of the instantaneous outward K-current towards more positive potentials. Mg2+, Zn2+ and Co2+ had qualitatively similar effects. Patch recordings with 150-160 mM K+-solution on both sides of the membrane revealed that the delayed outward K-current was carried through large conductance (250-300 pS) channels. Changes in free [Ca2+]i from 0 to 2 x 10(-8) M increased the activation of the large conductance K-channel. Small Na-currents were identified in cells from one cell line (Tp-378MG). The Na-conductance ranged from 0.5 to 7.5 nS in 25% of the cells, and was less than 0.5 nS in 75%. The Na-channels were activated and inactivated at 30-40 mV more positive potentials than in the mammalian peripheral nerve. Tetrodotoxin (100 nM) blocked gNa almost completely.

4-Aminopyridine↗
PubMed1989

Properties of appropriately and inappropriately expressed sodium channels in squid giant axon and its somata.

Neurons that form the giant axons in squid by axonal fusion in the stellate ganglion are inexcitable and do not express functional voltage-controlled sodium (Na) channels in their somata in vivo. These cells do express Na channels in the soma membrane in vitro, however, provided they have been axotomized. We describe here voltage-clamp experiments on the isolated cell bodies maintained in primary culture and on acutely isolated giant axons designed to compare the functional properties of the Na channels expressed inappropriately in the soma with those of channels expressed normally in the axon. Approximately 85% of Na channels in the soma are essentially indistinguishable from those in the giant axon with regard to gating properties and sensitivity to tetrodotoxin or saxitoxin. Thus, the isolated soma is capable of processing Na channels to a state of apparent functional perfection. In addition to these normal Na channels, another type is regularly expressed in the cultured somata. This second type lacks inactivation and is preferentially sensitive to block by cadmium ions, but is otherwise indistinguishable from the more prevalent normal type of channels.

Animals↗
PubMed1987

Nodes of Ranvier in acrylamide neuropathy: voltage clamp and electron microscopic analysis of rat sciatic nerve fibres at proximal levels.

Adult male rats were injected with acrylamide monomer (50 mg/kg i.p., 3 times/week). The animals developed hind limb paresis and distal motor nerve conduction velocity decreased. Three of 14 examined isolated myelinated sciatic nerve fibres showed a reduced excitability. In the remaining fibres the action potentials were normal. Potential clamp analysis of nodes of Ranvier in the single fibres revealed large delayed nodal K currents in 6 cases. Four of these 6 fibres exhibited a markedly increased membrane capacitance and in 2 fibres an increased Na permeability was found. Electron microscopic examination of sciatic nerves revealed comparatively subtle internodal and nodal-paranodal alterations in large myelinated fibres. Internodally, focal aggregates of tubulovesicular profiles could be found and some Schwann cells were hypertrophic. Paranodally, axonal evaginations penetrated in between the terminating myelin lamellae. Some paranodes had a very thin myelin covering and/or exhibited varying degrees of myelin sheath retraction. In the nodal axon domains lacking an axolemmal undercoating and partly non-undercoated axolemmal protrusions could be found. Similar physiological and morphological alterations occur in the rat sciatic nerve above a neuroma. Therefore, the presently observed proximal changes may, to some extent, represent non-specific alterations, secondary to a target deprivation caused by the distal axon degeneration typical for acrylamide neuropathy.

Acrylamide↗
PubMed1987

Voltage-clamp analysis of nodes of Ranvier in regenerated rat sciatic nerve.

Crush-lesioned adult rat sciatic nerves were allowed to regenerate during 70-181 days. Single large regenerated nerve fibres were isolated from levels distal to the crush site, and mounted in a feedback system for potential recordings and voltage clamp. After the experiment, each isolated fibre was fixed and embedded for morphological evaluation. Internodal lengths and fibre diameters were obtained form teased preparations of regenerated and normal sciatic nerves. The isolated regenerated fibres were excitable and had action potentials of large amplitude. TEA and 4-AP had negligible effects on the action potential and excitability properties. The time constant of the nodal segment was larger than in normal fibres. The nodal Na and K permeabilities (PNa and PK) were calculated both in absolute values and relative to the leak conductance (gL). Regenerated fibres had normal PNa/gL and PK/gL ratios. The potential dependence of PNa activation and inactivation was also normal. The isolated physiologically examined fibres had internodal lengths (L) of about 300 micron and diameters (D) of about 7-11 micron. In the teased fibre preparations L was about 300 micron (range 150-600 micron) and D was 3-11 micron. In addition, all teased regenerated nerve preparations exhibited a few scattered unusually short internodes (L less than 150 micron). In control nerves L ranged from 150 micron in the lower fibre size range (D = 2-3 micron) to 1.6 mm in the upper size range (D = 15 micron).

Action Potentials↗
PubMed1987

Reversible and irreversible nodal dysfunction in diabetic neuropathy.

Acute reversible diabetic nerve dysfunction has been associated with a reversible myo-inositol-related (Na+ + K+)-ATPase defect, while poorly reversible chronic nerve dysfunction correlates with progressive axoglial dysjunction of peripheral nerve. The causal relationships between biochemical and neuroanatomical abnormalities and those of nodal membrane function are not known. Nodal clamp examinations were carried out in the sciatic nerve of diabetic BB-rats to elucidate the events underlying diabetic nerve dysfunctions and how these relate to metabolic and structural defects of diabetic nerve. With increasing duration of diabetes, there was a progressive decline in nodal action potentials attributable to decreased Na+ permeability and a decrease in the membranous Na+ gradient. Vigorous insulin therapy in short-term (6-week) diabetic BB-rats normalized the Na+-permeability defect and the membranous Na+ gradient. These defects did not reverse in long-term (24-week) diabetic animals subjected to the same treatment. This poorly reversible nodal dysfunction accounts for the not readily reversible conduction defect in chronic diabetes and is probably directly related to irreversible axoglial dysjunction.

Animals↗
PubMed1987

T-lymphocyte subsets, functional deficits, and morphology in sciatic nerves during experimental allergic neuritis.

Conduction velocities, demyelination, "macrophage/dendritic" cells, different sets of T-lymphocytes, and immunoglobulins were estimated in sciatic nerves during various phases of experimental allergic neuritis in Lewis rats. Demyelination was minimal day 15 postimmunization (p.i.) when conduction velocity already was reduced, somewhat more pronounced day 17 p.i. when nerve conduction was blocked, and most pronounced day 23 p.i. when nerve conduction partially had recovered. This suggests a dissociation between the degree of demyelination and the functional deficits. Decrease of sciatic nerve conduction velocities coincided with endoneurial appearance of T-lymphocytes and "macrophage/dendritic" cells, as well as endoneurial immunoglobulins, day 15 p.i. Later partial functional recovery occurred in parallel with the disappearance of T-cells. The degree of functional deficits thus correlated with the number of endoneurial T-lymphocytes. T-cells may, directly or indirectly, initiate several of the disease components in experimental allergic neuritis, including the nerve conduction deficit.

Animals↗
PubMed1987

Synthesis of sodium channels in the cell bodies of squid giant axons.

Giant axons in squid are formed by fusion of axons from many small cell bodies in the giant fiber lobe (GFL) of the stellate ganglion. Somata of GFL cells in vivo are inexcitable and do not have measurable sodium current (INa) when studied with microelectrode or patch-electrode voltage-clamp techniques. If GFL cells are separated from the giant axons and maintained in primary culture, axon-like INa can be recorded from the somata after several days. Incorporation of Na channels into GFL cell bodies requires protein synthesis, intracellular microtubule-based transport, and the lack of a morphologically defined axon to serve as a sink for channels synthesized in culture.

Animals↗
PubMed1986

Nodes of Ranvier above a neuroma in the rat sciatic nerve: voltage clamp analysis and electron microscopy.

Neuroma formation was induced in adult rat sciatic nerves and the animals were allowed to survive for 1-10 months. In 10 animals single large myelinated fibres from the nerve segment above the neuroma were subjected to voltage clamp analysis. Six animals were fixed by glutaraldehyde perfusion and nodes of Ranvier or large myelinated fibres above the neuroma were examined in the electron microscope (EM). Most fibres exhibited normal action potentials, but a few had a reduced excitability and small action potentials. Some fibres had increased membrane time constant and leak conductance and a markedly increased membrane capacitance. Most of the examined nodes of Ranvier exhibited abnormally large delayed K currents, which could be blocked with 4-aminopyridine (4-AP). The Na current was normal. In the EM most large cross-cut myelinated axons were markedly atrophic, particularly after long survival times. Evaginations from the paranodal region of these axons penetrated between the terminating paranodal myelin lamellae. The nodal axolemmal undercoating could be very prominent and in some cases the nodal axon was irregular. These findings show that large myelinated peripheral nerve fibres, which are chronically disconnected from their peripheral targets, exhibit specific structural and functional abnormalities of the nodes of Ranvier.

Amputation Stumps↗
PubMed1985

Reversible diabetic nerve dysfunction: structural correlates to electrophysiological abnormalities.

Structural alterations of the nodal and paranodal areas were examined in the posterior tibial nerve in insulin-depleted and insulin-treated diabetic BB rats. The early metabolic phase of the distal symmetrical polyneuropathy was characterized by paranodal axonal swellings and nodal bulgings of the axon. These alterations correlate with intraaxonal sodium accumulation and decreased sodium equilibrium potentials which account for the early nerve conduction defect. Both the structural and electrophysiological abnormalities were completely normalized after vigorous insulin therapy. In the chronic diabetic polyneuropathy the paranodal area showed loss of paranodal axoglial junctions and paranodal myelin retraction. These changes may be partially responsible for the impaired electrical activity at the node as exemplified by irreversibly impaired sodium permeability and nerve conduction.

Animals↗