Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 323 (1983), S. 269-275 
    ISSN: 1432-1912
    Keywords: Palytoxin ; Tetraphenylphosphonium ; Depolarization ; Binding ; Borate ; Calcium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Palytoxin in concentrations as low as 10−11 to 10−12 M promotes the outflow of the lipophilic [3H]-tetraphenylphosphonium ion from particulate brain cortex of guinea-pigs and rats, and from preloaded crude synaptosomes of rats, which indicates depolarization. The outflow is not influenced by tetrodotoxin or the calcium channel blocker nimodipin, or by substitution of choline for Na+ ions. It is increased by Ca2+ and by borate, the latter interacting with the toxin itself. To assess the fixation of palytoxin to biological membranes, a binding step was installed before the depolarization step. Palytoxin binds to membranes from rat brain, liver, kidney, human and dog erythrocytes, and to a lesser degree to liposomes made from rat brain or erythrocyte lipids. Binding is reversible. It is decreased by mild physical pretreatments of crude synaptosomes. Palytoxin binding is increased in the presence of micromolar concentrations of Ca2+ or borate. It is concluded that the potentiation of palytoxin actions by Ca2+ or borate is at least partially due to the promotion of its binding.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 334 (1986), S. 1-9 
    ISSN: 1432-1912
    Keywords: Depolarization ; Ion channels ; Phosphatidylinositol ; Inositol phosphates ; Voltage-dependence
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have studied the accumulation of inositol phosphates (InsP) due to depolarization. A particulate preparation of rat brain was introduced to rule out transmitter activated mechanisms and to allow free access for drugs of high molecular weights. Potassium depolarization doubled InsP within a few minutes. InsP accumulation depended on time and K+ concentration, and was affected neither by tetrodotoxin nor by atropine. Radioactive metabolites co-eluted with inositol mono-phosphate and inositol bis-phosphate, whereas only minor amounts appeared with inositol tris-phosphate. The content in phosphatidylinositols was decreased. No evidence was found for the involvement of a neurotransmitter. Sea anemone toxin II (around 1 μmol/l), which keeps the Na+-channels open, promoted the InsP accumulation in an atropine-resistant manner. Tetrodotoxin prevented it when given before, and inhibited it when given after initiation by sea anemone toxin II. Moreover the K+ channel blockers 4-aminopyridine, dendrotoxin and tetraethylammonium all caused InsP accumulation. Palytoxin was by far the most potent promoter of InsP accumulation with a detection limit below 10 pmol/l, and displayed a unique bell-shaped concentration-effect correlation. Ouabain (3 μmol/l) and above) also elicited the InsP accumulation. The response to carbachol was not only inhibited completely by atropine, but also partially (more than 50%) by tetrodotoxin, which indicates the involvement of voltage-dependent sodium channels in the receptor-triggered InsP accumulation. Thus independent of the causative agent, depolarization promotes an InsP accumulation. We conclude that degradation of phosphatidylinositols is mediated not only by receptor occupation but also by a positive shift in membrane voltage.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 330 (1985), S. 77-83 
    ISSN: 1432-1912
    Keywords: Dendrotoxin ; Potassium channel ; Nerve fibre ; Depolarization ; GABA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of dendrotoxin (DTX), a toxic peptide from Dendroaspis angusticeps venom, were studied electrophysiologically on peripheral frog nerve fibres, and biochemically on large synaptosomes from rat brain. 1. On nerve fibres, DTX reduced the amplitude and prolonged the duration of the action potential; even at 0.1 nmol/l DTX produced significant effects. Maximum block of potassium currents occurred at about 30 nmol/l. Turning on of the remaining current was slowed. Reversibility was incomplete. The reduction of potassium currents was between 31% and 85% at 85 nmol/l DTX (n=8). The remainder appeared to be resistant to DTX. Sodium channels were not affected. 2. On large synaptosomes DTX (above 1 nmol/l) produced a slight depolarization, indicated by an outward shift of the lipophilic cation tetraphenylphosphonium, and promoted the release of radioactivity after preloading with [3H] GABA. DTX had similar potency but lower efficacy in this respect than sea anemone toxin II (ATX II). In contrast to the effects of ATX II, those due to DTX were only partially inhibited by tetrodotoxin. The actions of 4-aminopyridine resembled those of DTX, but the latter was about 500 times more potent. The electrophysiological data provide direct evidence for blockade of a potassium channel by DTX. This action is sufficient to explain the biochemical observations, although additional effects on synaptosomes cannot be excluded.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...