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PubMed1990

Action of cromakalim on potassium membrane conductance in isolated heart myocytes of frog.

1. The effects of cromakalim on membrane currents were studied at 20 degrees C in frog atrial and ventricular cells in patch clamp recording using the whole cell configuration. 2. When cromakalim (1 microM) was applied in the external medium, a time-independent current was activated in a few minutes. Cromakalim induced a weak increase of inward membrane currents recorded during hyperpolarization and a large increase of outward membrane currents recorded during depolarization. 3. The current voltage relationship of the cromakalim-induced current reversed near EK and rectified in the outward direction. 4. The cromakalim-activated current was inhibited by external application of cesium (20 mM), barium (1.8 mM), tolbutamide (1 mM) and glibenclamide (1 microM). 5. The effects of cromakalim were insensitive to a cytosolic increase in adenosine 5'-triphosphate (ATP, 3-5 mM). Cromakalim had no effects when applied in the cell. 6. Our results confirm that cromakalim activates an IK(ATP)-like conductance and suggest that the effects of the drug are due to an action on the external side of the membrane and are independent of the ATP cell content.

Adenosine Triphosphate↗
PubMed1980

Electrophysiological properties of in vitro Purkinje cell somata in mammalian cerebellar slices.

1. The electrical activity of Purkinje cells was studied in guinea-pig cerebellar slices in vitro. Intracellular recordings from Purkinje cell somata were obtained under direct vision, and antidromic, synaptic and direct electroresponsiveness was demonstrated. Synaptic potentials produced by the activation of the climbing fibre afferent could be reversed by direct membrane depolarization. 2. Input resistance of impaled neurones ranged from 10 to 19 M omega and demonstrated non-linearities in both hyperpolarizing and depolarizing directions. 3. Direct activation of a Purkinje cell indicated that repetitive firing of fast somatic spikes (s.s.) occurs, after a threshold, with a minimum spike frequency of about 30 spikes/sec, resembling the '2-class' response of crab nerve (Hodgkin, 1948). 4. As the amplitude of the stimulus was increased, a second form of electroresponsiveness characterized by depolarizing spike bursts (d.s.b.) was observed and was often accomppanied by momentary inactivation of the s.s. potentials. Upon application of tetrodotoxin (TTX) or removal of Na+ ions from the superfusion fluid, the s.s. potentials were abolished while the burst responses remained intact. However, Ca conductance blockers such as Co, Cd, Mn and D600, or the replacement of Ca by Mg, completely abolish d.s.b.s. 5. If Ca conductance was blocked, or Ca removed from the superfusion fluid without blockage of Na conductance, two types of Na-dependent electroresponsiveness were seen: (a) the s.s. potentials and (b) slow rising all-or-none responses which reached plateau at approximately -15 mV and could last for several seconds. These all-or-none Na-dependent plateau depolarizations outlasted the stimulus and were accompanied by a large increase in membrane conductance. Within certain limits the rate of rise and amplitude of the plateau were independent of stimulus strength. The latency, however, was shortened as stimulus amplitude was increased. These potentials were blocked by TTX or by Na-free solutions. 6. Substitution of extracellular Ca by Ba or intracellular injection of tetraethylammonium generated prolonged action potentials lasting for several seconds and showing a plateau more ositive than those obtained in norrmal circumstances by either non-inactivating Na or Ca currents. 7. Spontaneous firing of the Purkinje cell was characterized by burst-like activity consisting of both s.s. and d.s.b. responses. Addition of TTX to the bath left the basic spontaneous activity and its frequency unaltered, indicating tha Ca spiking and Ca-dependent K conductance changes are the main events underlying this oscillatory behaviour. 8...

Action Potentials↗
PubMed1983

Persistent slow inward calcium current in voltage-clamped hippocampal neurones of the guinea-pig.

CA1 and CA3 neurones in transverse slices of guinea-pig hippocampus were voltage clamped through a single micro-electrode, and perfused with Krebs solution containing 0.5 microM-tetrodotoxin and 10 mM-tetraethylammonium at (normally) 24-26 degrees C. Slow inward currents of less than or equal to 0.5 nA were recorded during depolarizing voltage commands to membrane potentials positive to between -40 and -30 mV. These currents peaked at 100-300 msec after the onset of the depolarizing command, then subsequently declined during continuing depolarization. This decline could be ascribed to a developing outward current since repolarizing inward current tails showed no diminution up to 700 msec. No clear evidence for time-dependent inactivation of the inward current could be obtained. A persistent component of inward current could be detected when the membrane potential was maintained above the inward current threshold, such that small hyperpolarizing commands induced an outward relaxation and large hyperpolarizations produced an inward tail current. The inward current was depressed by removing external Ca, or by adding 0.2-0.5 mM-Cd, or 0.1 mM-verapamil, and was increased by adding 1 mM-Ba. A possible role for this persistent inward current in generating the slow membrane depolarization underlying burst discharges in these neurones is discussed. In some neurones (primarily CA1), an additional fast spike-like current was recorded, which was blocked by Cd or Mn and depressed by a depolarizing pre-pulse. It is suggested that this was a manifestation of the previously-reported dendritic Ca spike.

Action Potentials↗
PubMed1983

Ion currents in Drosophila flight muscles.

1. The dorsal longitudinal flight muscles of Drosophila melanogaster contain three voltage-activated ion currents, two distinct potassium currents and a calcium current. The currents can be isolated from each other by exploiting the developmental properties of the system and genetic tools, as well as conventional pharmacology.2. The fast transient potassium current (I(A)) is the first channel to appear in the developing muscle membrane. It can be studied in isolation between 60 and 70 hr of pupal development. The channels can be observed to carry both outward and inward currents depending on the external potassium concentration. I(A) is blocked by both tetraethylammonium ion (TEA) and 3- or 4-aminopyridine. The inactivation and recovery properties of I(A) are responsible for a facilitating effect on membrane excitability.3. The delayed outward current (I(K)) develops after maturation of the I(A) system. I(K) can be isolated from I(A) by use of a mutation that removes I(A) from the membrane current response and can be studied before the development of Ca(2+) channels. I(K) shows no inactivation. The channels are more sensitive to blockage by TEA than I(A) channels, but are not substantially blocked by 3- or 4-aminopyridine.4. The calcium current (I(Ca)) is the last of the major currents to develop and must be isolated pharmacologically with potassium-blocking agents. I(Ca) shows inactivation when Ca(2+) is present but not when Ba(2+) is the sole current carrier. When Ca(2+) is the current carrier, the addition of Na(+) or Li(+) retards the inactivation of the net inward current. When the membrane voltage is not clamped, Ba(2+) alone, or Ca(2+) with Na(+) (or Li(+)), produces a plateau response of extended duration.5. The synaptic current (I(J)) evoked by motoneurone stimulation is the fastest and largest of the current systems. It has a reversal potential of approximately -5 mV, indicating roughly equal permeabilities of Na(+) and K(+). During a nerve-driven muscle spike, I(J) is the major inward current, causing a very rapid depolarization away from resting potential. An exceptionally large synaptic current is necessary to rapidly discharge the high membrane capacitance (0.03 muF/cell) in these large (0.05 x 0.1 x 0.8 mm) isopotential cells.

Aminopyridines↗
PubMed1985

The slow calcium-dependent potassium current in a myenteric neurone of the guinea-pig ileum.

Experiments were performed in current-clamped and voltage-clamped after-hyperpolarizing (AH) neurones of the guinea-pig myenteric plexus to examine the properties of the potassium conductance (gK, Ca) underlying the slow calcium-activated after-hyperpolarization (VK, Ca). The action potential plateau lengthened by the addition of tetraethylammonium chloride (TEA) to the bathing medium was compared to VK, Ca. Results were consistent with enhanced calcium entry causing an increase of VK, Ca. 4-Aminopyridine (4-AP) directly reduced VK, Ca. Voltage-clamp data of gK, Ca were well fitted by a process with a delay (approximately equal to 60 ms) followed by exponential activation (time constant approximately equal to 300 ms) and inactivation (time constant approximately equal to 2 s). The presence of a small, much slower inactivating process was noted. Values for time constants were similar to those reported by Morita, North & Tokimasa (1982) and North & Tokimasa (1983) where gK, Ca was measured during VK, Ca subsequent to action potential stimulation. The relation between gK, Ca (or the calcium-activated potassium current IK, Ca) and estimated calcium influx resulting from short-duration calcium currents elicited at various voltages was compared. Both the integral of the calcium current and gK, Ca showed a similar dependence on the depolarizations used to elicit IK, Ca except there was a positive shift of about 4 mV for the gK, Ca curve. This shift was attributed to a requirement for calcium ions to prime the gK, Ca mechanism. An inward ion charge movement of about 8 pC was required before significant activation of gK, Ca occurred. After the 'priming' condition had been established, the sensitivity of gK, Ca to inward calcium current measured at the resting potential was about 500 pS/pC of inward charge. Large calcium entry obtained by prolonged calcium currents caused saturation of the peak amplitude of IK, Ca and initiated currents with slower time to peak amplitude and longer duration. Increasing the calcium concentration of the external solution provided proportionally larger IK, Ca currents before saturation. The saturation amplitude of IK, Ca (namely gK, Ca) was relatively unaffected.

4-Aminopyridine↗
PubMed1987

Function and distribution of three types of rectifying channel in rat spinal root myelinated axons.

1. The nature, distribution and function of rectifying channels in rat spinal root myelinated axons has been assessed with selective blocking agents and a variety of intracellular and extracellular recording techniques. 2. The electrotonic responses of roots poisoned with tetrodotoxin (TTX) to constant current pulses had fast (rise time much less than 1 ms) and slow components, which were interpreted in terms of Barrett & Barrett's (1982) revised cable model for myelinated nerve. Depolarization evoked a rapid outward rectification (time constant, tau approximately 0.5 ms), selectively blocked by 4-aminopyridine (4AP, 1 mM), and a slow outward rectification (tau approximately 15 ms), selectively blocked by tetraethylammonium (TEA, 1 mM) or Ba2+ (0.5 mM). Hyperpolarization evoked an even slower inward rectification, selectively blocked by Cs+ (3 mM) but not by Ba2+. 3. From the different effects of the blocking agents on the fast and slow components of electrotonus, it was deduced (a) that the inward rectification is a property of the internodal axon, (b) that the slow outward rectifier is present at the nodes, and probably the internodes as well, and (c) that the 4AP-sensitive channels have a minor nodal and a major internodal representation. 4. TEA and Ba2+ reduced the accommodation of roots and fibres not poisoned with TTX to long current pulses, whereas 4AP facilitated short bursts of impulses in response to a single brief stimulus. 5. TEA and Ba2+ also abolished a late hyperpolarizing after-potential (peaking at 20-80 ms), while 4AP enhanced the depolarizing after-potential in normal fibres, and abolished an early hyperpolarizing after-potential (peaking at 1-3 ms) in depolarized fibres. Corresponding to the later after-potentials were post-spike changes in excitability and conduction velocity, which were affected similarly by the blocking agents. Cs+ increased the post-tetanic depression attributable to electrogenic hyperpolarization. 6. The physiological roles of the three different rectifying conductances are discussed. It is also argued that the prominent ohmic 'leak conductance', usually ascribed to the nodal axon, must arise in an extracellular pathway in series with the rectifying internodal axon.

4-Aminopyridine↗
PubMed1987

Patch-clamp study of the calcium-dependent chloride current in AtT-20 pituitary cells.

1. Voltage-clamp recordings were made from cultured AtT-20 pituitary cells using the whole-cell patch-clamp technique. Cells were perfused internally with Cs+ to block K+ currents and bathed externally with either 1 microM tetrodotoxin or with tetraethylammonium (TEA) as a Na+ substitute to block voltage-activated Na+ currents. 2. Depolarizing voltage steps from a holding potential of -80 mV to potentials positive to -30 mV evoked two currents: a fast inward current that activated between -30 and +70 mV and a slowly activating current (designated "slow step current") that was inward between -30 and near 0 mV (the Cl- equilibrium potential) and outward positive to about 0 mV. Repolarization to -80 mV revealed a slowly decaying, inward tail current, whose magnitude with respect to step potential closely matched the current-voltage relationship of the voltage-activated Ca2+ current. 3. Activation of the fast inward current, slow step current, and tail current, was prevented by extracellular application of Cd2+ or removal of extracellular Ca2+. Replacement of extracellular Ca2+ with Ba2+ potentiated the fast inward current but blocked the slow step and tail currents. Intracellular perfusion with greater than 1 mM of the Ca2+ chelators ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid (EGTA) or [1,2-bis(2)aminophenoxy]ethane N,N,N',N'-tetraacetic acid (BAPTA) prevented activation of the slow step and tail currents, but not the fast inward current. 4. The reversal potential of the slow inward current was sensitive to changes in the Cl- equilibrium potential but not to substitution of TEA for Na+. The slow step current, but not the fast inward current, was partially blocked by the Cl- channel blocker, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid. 5. These data indicate that both the slow inward tail current and the slowly activating, reversible step current were a Ca2+-dependent Cl- current, similar to that described in other neuronal and nonneuronal cell types. The fast inward current was a voltage-activated Ca2+ current, described previously in these and other cells. 6. In the absence of intracellular EGTA, the tail current decayed with complex kinetics, its time course apparently dependent on the magnitude of the voltage-activated Ca2+ current. In the presence of 200 microM intracellular EGTA, the tail current decayed significantly faster and often decayed exponentially.

Animals↗
PubMed1979

Action potential generation in reaggregates of rat aortic smooth muscle cells in primary culture.

Cultured vascular smooth muscle cells were prepared from adult rat aortas. The cells were dispersed by collagenase/elastase, and allowed to reaggregate into small spheres (50-200 micron in diameter) by plating on to cellophane. These primary cultures were incubated for 5-14 days, and then impaled with microelectrodes. The mean resting potential was -55 mV, and the mean input resistance was 9.0 M omega. The cells were quiescent, electrically and mechanically, and electrical stimulation usually did not elicit responses. However, addition of Ba++ (1 mM) or tetraehtylammonium ion (TEA; 5-15 mM) induced excitability (with accompanying contractions), either as spontaneous action potentials or by allowing responses to electrical stimulation. The cells became partially depolarized (e.g., to -36 mV) by these agents, and the input resistance increased. The frequency of spontaneous firing of the Ba++-induced spikes was affected by polarizing current pulses, as expected for pacemaker behavior. Elevation of Ca++ in the bathing solution increased the amplitude (overshoot) of the action potentials, and the spikes were blocked by verapamil (10(-5) M). Electron microscopy showed that the reaggregates consisted of a tight packing of elongated small-diameter cells, some of which exhibited thick and thin myofilaments and 'dense bodies'; many cells possessed surface caveolae. The results of this study demonstrate that reaggregates of arterial smooth muscle in primary culture can maintain functional and morphological characteristics of intact arterial smooth muscle, and therefore provide a useful preparation for the study of vascular smooth muscle function and control.

Action Potentials↗
PubMed1976

A 'TEA+-insensitive' mutant with increased potassium conductance in Paramecium aurelia.

A single-gene mutant of Paramecium aurelia is analysed electrophysiologically. (a) The regenerative Ca-response, triggered by small or moderate current, was smaller and slower in the mutant than in wild type. (b) Input resistance of the mutant membrane is about half of that of wild type bathed in various solutions. This is true for the zero-current input resistance and the chord resistance measured with high depolarizing current. (c) Membrane resistance of the mutant measure with hyperpolarizing currents is smaller than that of wild type only when K+ is the major external cation. (d) Internally applied TEA+ or externally applied Ba+ increases the membrane resistance of the mutant to that of wild type similarly treated. We conclude that the mutant has an increased K conductance.

Action Potentials↗
PubMed1975

Pharmaco-radiology in barium examinations with special reference to glucagon.

The reasons for and objections to the use of drugs as adjuncts in barium meal and follow-through examinations are briefly reviewed. Physiological factors related to gastric emptying are considered, including the volume, temperature and osmolarity. The drugs considered include those that speed gastric emptying and small bowel transit such as metoclopramide, those that delay gastric emptying such as propantheline and gastrointestinal hormones such as glucagon. Glucagon first produces gastric and duodenal dilatation and subsequently speeds transit through the small bowel. The indications, contra-indications and side effects of these drugs are also considered and tabulated.

Barium Sulfate↗
PubMedDate not supplied

[Pharmacological research on bonnecor and its metabolites].

The antiarrhythmic and local anesthetic effects of 4 metabolites (G 491, ABD 19-200, ABD 19-199, ABD 19-205) of a new antiarrhythmic drug bonnecor (GS-015) were studied on the models of arrhythmias induced by aconitine (rats), barium chloride (rabbits), electrical fibrillation (cats), ouabain (dogs) as well as surface anesthesia (rabbit cornea). The side effects on the cardiovascular system were investigated on anesthetized cats. As compared with the original compound (bonnecor) metabolites G 491 and ABD 19-200 on different test models exhibited the action which on the antiarrhythmic terms was 2-14 times less weak than that of bonnecor but the metabolites were less toxic. Metabolites ABD 19-199 and ABD 19-205 reach the degree of effectiveness of bonnecor but their toxicity is higher. It follows from the above that the beneficial effect of bonnecor is not achieved by its metabolites.

Animals↗
PubMed1988

Effects of 2-(4-phenylpiperidino)cyclohexanol (AH5183) and barium ions on frog neuromuscular transmission.

1. By applying electrophysiological techniques such as frequency facilitation, tetanic run-down and depression, recovery from depression and post-tetanic potentiation (PTP) of the end-plate potential (EPP), the effects on frog neuromuscular transmission of 2-(4-phenylpiperidino)cyclohexanol (AH5183), a compound known to inhibit specifically the loading of newly synthesized acetylcholine (ACh) molecules into synaptic vesicles, and Ba2+, a selective activator of the augmentation phase of PTP, were investigated to elucidate whether these were related to ACh turnover. 2. Effects of AH5183 and Ba2+ ions were frequency dependent. At low frequency of stimulation, both agents showed essentially no effects on the EPPs recorded from Mg2+-blocked preparations. 3. AH5183 pivoted the log-linear frequency facilitation relation clockwise without altering the intercept on the ordinate, whereas Ba2+ ions did so counter-clockwise. As is the case with Ca2+ ions, Sr2+ ions shifted the relation upwards leaving its slope unaffected. 4. AH5183 selectively depressed the component of potentiation in PTP while the effect of Ba2+ ions was a specific increase in the augmentation phase of PTP. 5. Ba2+ ions increased the amplitude of EPPs in the late depressed phase during the tetanic run-down and depression experiment, but 4-aminopyridine and Ca2+ ions failed to do so. 6. AH5183 increased, Ba2+ ions reduced but Ca2+ ions did not change the constant of recovery from depression of the EPP measured on curarized preparations. 7. The present results suggested that mobilization of the ACh quanta readily available for release might be a common mechanism underlying both frequency facilitation and two components of PTP (augmentation and potentiation). The term 'frequency facilitation' would be more comprehensive if it were re-termed 'frequency augmentation' or 'frequency potentiation'.

4-Aminopyridine↗
PubMed2000

Strontium selenogermanate(III) and barium selenogermanate(II,IV): synthesis, crystal structures, and chemical bonding

The new selenogermanates Sr2Ge2Se5 and Ba2Ge2Se5 were synthesized by heating stoichiometric mixtures of binary selenides and the corresponding elements to 750 degrees C. The crystal structures were determined by single-crystal X-ray methods. Both compounds adopt previously unknown structure types. Sr2Ge2Se5 (P2(1)/n, a = 8.445(2) A, b = 12.302 A, c = 9.179 A, beta = 93.75(3) degrees, Z = 4) contains [Ge4Se10]8- ions with homonuclear Ge-Ge bonds (dGe-Ge = 2.432 A), which may be described as two ethane-like Se3Ge-GeSeSe2/2 fragments sharing two selenium atoms. Ba2Ge2Se5 (Pnma, a = 12.594(3) A, b = 9.174(2) A, c = 9.160(2) A, Z = 4) contains [Ge2Se5]4- anions built up by two edge-sharing GeSe4 tetrahedra, in which one terminal Se atom is replaced by a lone pair from the divalent germanium atom. The alkaline earth cations are arranged between the complex anions, each coordinated by eight or nine selenium atoms. Ba2Ge2Se5 is a mixed-valence compound with GeII and GeIV coexisting within the same anion. Sr2Ge2Se5 contains exclusively GeIII. These compounds possess electronic formulations that correspond to (Sr2+)2(Ge3+)2(Se2-)5 and (Ba2+)2- Ge2+Ge4+(Se2-)5. Calculations of the electron localization function (ELF) reveal clearly both the lone pair on GeII in Ba2Ge2Se5 and the covalent Ge-Ge bond in Sr2Ge2Se5. Analysis of the ELF topologies shows that the GeIII-Se and GeIV-Se covalent bonds are almost identical, whereas the GeII-Se interactions are weaker and more ionic in character.

Journal Article↗