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C Cognard

Publications and source records attributed to C Cognard.

105 records · Page 6Linked to original sources
PubMed1986

Tetrodotoxin-sensitive and tetrodotoxin-resistant Na+ channels differ in their sensitivity to Cd2+ and Zn2+.

The sensitivity of Na+ channels to inhibition by Cd2+ and Zn2+ was studied in 22Na+ uptake experiments after stabilization of an open conformation of the Na+ channels with different neurotoxins and in voltage clamp experiments. Six different cell types of neuronal, cardiac or skeletal muscle origin were surveyed. Three cell types possess Na+ channels that are highly sensitive to tetrodotoxin (TTX) (Kd = 1-5 nM) and three possess Na+ channels that are resistant to TTX (Kd = 0.3-1 microM). The 22Na+ uptake experiments using veratridine or batrachotoxin to activate Na+ channels indicated that TTX-resistant Na+ channels are more sensitive to the inhibitory action of Cd2+ (IC50(Cd2+) = 0.2 mM) and of Zn2+ (IC50(Zn2+) = 50 microM) than TTX-sensitive Na+ channels (IC50(Cd2+) = 5 mM, IC50(Zn2+) = 2 mM). Electrophysiological experiments showed that high concentrations of Cd2+ (IC50 = 2 mM) are necessary to inhibit both TTX-sensitive and TTX-insensitive Na+ channels when the channels are activated by voltage steps. The results suggest that Cd2+ acts competitively with veratridine or batrachotoxin and that the difference in the effects of Cd2+ and Zn2+ on 22Na+ fluxes in TTX-sensitive and TTX-resistant cells is related to differences at the site of action of alkaloid neurotoxins.

Animals↗
PubMed1986

The voltage-dependent blocking effect of phalloidin on the delayed potassium current of voltage-clamped frog skeletal muscle fibres.

The effects of phalloidin (10(-14)-10(-6) M) were tested on voltage-clamped isolated frog muscle fibres. The toxin reversibly blocked the potassium current similarly in both detubulated and intact fibres. Neither the reversal potential nor the activation curve of the current were affected by the toxin (10(-8) M). The inactivation curve was shifted toward negative values at holding potentials more than +20 mV from the reference potential. This shift enhanced the potential-dependent facilitation of the current block observed between -40 and +40 mV from the reference holding potential (the higher the depolarization, the greater the blocking effect, which reached 100% at +40 mV). Contrary to what was seen with the current, hyperpolarization did not relieve the mechanical block. The effect of phalloidin did not seem to be frequency-dependent.

Animals↗
PubMed1986

The apamin-sensitive potassium current in frog skeletal muscle: its dependence on the extracellular calcium and sensitivity to calcium channel blockers.

Slow outward potassium currents were recorded in isolated frog skeletal muscle fibres using the double mannitol-gap voltage-clamp technique. Detubulated fibres failed to generate a slow outward current, and apamin had no effect on the remaining current. The maximum blocking effect of organic and inorganic Ca2+-channel blockers on the slow outward channels of intact fibres was larger than that of apamin. Apamin failed to induce an additional block when applied after Ca2+-channel blockers. In a low-Ca2+ solution (OCa, EGTA 1 mM) the slow outward current was slightly increased and the blocking effect of apamin was enhanced. A Ca2+-rich solution (Ca2+ X 10) increased the slow outward current and the blocking effect of apamin was drastically reduced. It is concluded that the apamin-sensitive current which is a component of the slow outward K+ current is located in the tubular membrane. Its activation seems barely dependent on the Ca2+ influx via the slow inward Ca2+ current. Apamin-receptor binding appears to be dependent on the extracellular Ca2+ concentration. Blockade of slow outward current by Ca2+-channel blockers is likely to be the result of a direct action on the slow K+ permeability rather than a consequence of Ca2+ channel inhibition.

Animals↗
PubMed1986

Bay K 8644 enhances slow inward and outward currents in voltage-clamped frog skeletal muscle fibres.

In isolated frog skeletal muscle fibre slow inward calcium current and slow outward potassium current were recorded by means of a double mannitol-gap device. Bay K 8644, the so-called Ca-channel activator, shifted the activation threshold of the slow inward calcium current (recorded in Cl-free, Ca-rich solution), towards negative potential by 15 mV. It increased the peak current amplitude in a dose-dependent manner (from 10(-11) to 10(-7) M; EC50 approximately equal to 10(-9) M). Apamin, the bee venom toxin which is known to specifically block a class of calcium-dependent potassium channels, failed to block the slow inward calcium current and slowed down its declining phase. This effect exhibited a potential dependence: the more the membrane was depolarized, the more the current decay was slowed down. Bay K 8644 (10(-7) M) transiently decreased the slow outward potassium current, which then progressively increased to stabilize at 135% of the control value. This effect seemed to be more pronounced at potentials above the reversal potential for inward ICa. The results suggest that the increase of the slow outward current is due to a direct action of Bay K 8644 on the slow K channel, rather than an indirect action via potentiation of slow inward calcium current. Moreover, results obtained with apamin indicated that the slow outward potassium current is unlikely to flow through Ca-channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1986

Different types of Ca2+ channels in mammalian skeletal muscle cells in culture.

This paper describes the existence of two pharmacologically distinct types of Ca2+ channels in rat skeletal muscle cells (myoballs) in culture. The first class of Ca2+ channels is insensitive to the dihydropyridine (DHP) (+)-PN 200-110; the second class of Ca2+ channels is blocked by low concentrations of (+)-PN 200-110. The two pharmacologically different Ca2+ channels are also different in their voltage and time dependence. The threshold for activation of the DHP-insensitive Ca2+ channel is near -65 mV, whereas the threshold for activation of the DHP-sensitive Ca2+ channel is near -30 mV. Current flowing through the DHP-insensitive Ca2+ channel is transient with relatively fast kinetics. Half-maximal inactivation for the DHP-insensitive Ca2+ channel is observed at a holding potential Vh0.5 = -78 mV and the channel is completely inactivated at -60 mV. Two different behaviors have been found for DHP-sensitive channels with two different kinetics of inactivation (one being about 16 times faster than the other at -2 mV) and two different voltage dependencies. These two different behaviors are often observed in the same myoball and may correspond to two different subtypes of DHP-sensitive Ca2+ channels or to two different modes of expression of one single Ca2+ channel protein.

Animals↗
PubMed1986

Dihydropyridine-sensitive Ca2+ channels in mammalian skeletal muscle cells in culture: electrophysiological properties and interactions with Ca2+ channel activator (Bay K8644) and inhibitor (PN 200-110).

The whole-cell patch-clamp technique has been used to analyze the properties of the dihydropyridine-sensitive Ca2+ channel in rat skeletal muscle cells (myoballs) in culture. The potential dependence of Ca2+-channel activation is similar to that observed in cardiac cells. However, the skeletal muscle Ca2+ channel is activated more slowly (by a factor of about 10). The voltage dependence of Ca2+-channel inactivation indicates a half-maximal inactivation (Vh0.5) at -72 mV as compared to Vh0.5 = -35 mV for cardiac cells. Blockade of the skeletal muscle Ca2+ channel by the dihydropyridine (+)-PN 200-110 is voltage dependent, with a half-maximal effect (K0.5) of 13 nM for an application of the drug to the myoball membrane held at -90 mV and of 0.15 nM for an application at a potential of -65 mV. The 100-fold difference in apparent affinity is interpreted as a preferential association of PN 200-110 with the inactivated form of the Ca2+ channel. The K0.5 value found from electrophysiological experiments for the binding to the inactivated state (K0.5 = 0.15 nM) is nearly identical to the equilibrium dissociation constant found from binding experiments with (+)-[3H]PN 200-110 using transverse-tubular membranes (Kd = 0.22 nM). The dihydropyridine activator Bay K8644 acts by increasing Ca2+ current amplitude and by slowing down deactivation.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1985

The strontium-induced calcium-release process and its implication in contractility of skeletal muscle of Rana ridibunda.

The electrical and mechanical activities of isolated frog muscle fibres have been recorded simultaneously under conditions (chloride-free saline containing 78.5 mM strontium acetate substituting for NaCl and CaCl2) that allow the development of a tubular strontium permeability. Under voltage-clamp conditions a large part of the contraction is due to the slow inward ISr since both are inhibited by Ni (10 mM). The remaining component of contraction, which seems to be potential-dependent, is not abolished by tetracaine (40 microM) which blocks the current-dependent component. A cumulative effect of strontium, which is not observed in the presence of Ni, leads to a 60-80% reduction in contractility for an estimated [Sr]i near 3 X 10(-4) M while the ending of the contraction observed when Sr is replaced by Ba is never obtained. In contrast no cumulative effect is observed when Ca substitutes for Sr. The first evoked inward current following a caffeine contracture fails to elicit a contraction, but in Ringer 78.5 Sr, contractility is progressively restored by successive depolarizations up to an amplitude which corresponds to 25-40% of the maximum activity. In the presence of Ca instead of Sr, the restoration of contractility reaches 100%. This recovery does not occur when the inward current is blocked by Ni. After strontium loading, a calcium entry fails immediately and reversibly to induce a mechanical response while barium ions induce a progressive and irreversible block of contractility. These results suggest that the strontium entry during successive depolarizations leads to a progressive replacement of intrareticular calcium by strontium. When all the calcium ions have been substituted for by strontium ions, the contractile apparatus remains capable of being activated by intrareticular strontium.

Animals↗
PubMed1985

Effects of phalloidin on electrical and mechanical activity of frog muscle fibres.

The effects of phalloidin (10(-15) to 10(-5) M) on isolated muscle fibres of the frog were investigated under current or voltage clamp conditions in a double mannitol gap device coupled to a mechanoelectric transducer which allowed the estimation of isometric tension. The toxin significantly increased the action potential duration and the amplitude of the associated contraction. Under voltage-clamp conditions, for a concentration range of 10(-14) to 10(-8) M, phalloidin reversibly decreased (up to 42.7% +/- 3.1) the fast outward potassium current responsible for the delayed rectification. For concentrations from 10(-8) to 10(-5) M, the toxin irreversibly reduced (up to 43.3% +/- 2.9) the amplitude of the contractile response. It is concluded that, in skeletal muscle fibre of frog, phalloidin acts at two different levels, one which may be located at the outer face of the surface membrane while the other may be located deeper within the cell.

Action Potentials↗
PubMed1984

Effects of apamin on the outward potassium current of isolated frog skeletal muscle fibres.

The effect of apamin, a polypeptidic toxin from bee venom which is a specific blocker of certain Ca2+-dependent K+ channels, has been tested (50-100nM) on voltage clamped single skeletal muscle fibres of the frog. The results have shown the existence of an inhibitory effect of the toxin on the slow outward K+ current which suggests the existence of a Ca2+-sensitive component of the slow K+ permeability in the plasma membrane of the frog muscle fibre.

Animals↗
PubMed1983

[Permeability to strontium ions and excitation-contraction coupling in skeletal muscle of frogs].

Electrical and mechanical activities of frog skeletal muscle fibres were simultaneously investigated under conditions which allow the development of a strontium permeability. It was shown that the contraction elicited by a long lasting Sr response depends upon two mechanisms: a potential dependent one, and a mechanism which is related to the entry of Sr ions into the cell through the tubular membrane.

Animals↗
PubMedDate not supplied

Paraspinal arteriovenous fistula with perimedullary venous drainage.

A paravertebral presacral posttraumatic arteriovenous fistula drained through the ascending lumbar vein to the epidural plexuses and perimedullary veins. The patient did not have symptoms of myelopathy, only low-back pain and radicular hypoesthesia. The lesion was embolized with a large balloon and clinical symptoms disappeared.

Adolescent↗
PubMedDate not supplied

[Persistent value of intra-arterial fibrinolysis 8 hours or more following central retinal artery occlusion or of its branches].

PURPOSE: To establish that intra-arterial fibrinolysis of the ophthalmic artery can still be efficient 8 hours or more after a central retinal artery occlusion. MATERIAL AND METHODS: Nine to twenty hours (average 12.5 H) after a loss of vision due to a central retinal artery occlusion or the occlusion of its branches, 7 patients were treated by intra-arterial fibrinolysis. The vision of the affected eye was limited to light perception for four patients, to hand movement at 1 meter for two patients, and to 4/10 P2 for one patient. Under radiological guidance, 300.000 IU of urokinase was injected through a microcatheter placed in the ophthalmic artery (6 patients), or in the facial artery (1 patient); in this case the angiogram showed an occlusion of the internal carotid artery and a retrograde filling of the ophthalmic artery through the facial artery. RESULTS: We did not observed any complication. The 3 patients who had a vision better than light perception recovered a vision of 10/10 P2. For the others: two patients recovered a vision of 9/10 P2 and 5/10 P2, two did not recover. CONCLUSION: Fibrinolysis of the ophthalmic artery must ideally be performed as soon as possible, but a recovery is still possible more than 8 hours after the onset of the loss of vision. The time limit is not yet defined but after 24 hours, the chance of improvement seems to be very low.

Adult↗