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P Arhem

Publications and source records attributed to P Arhem.

At least 55 records · Page 3Linked to original sources
PubMed1989

A model for the fast 4-aminopyridine effects on amphibian myelinated nerve fibres. A study based on voltage-clamp experiments.

The effect of 4-aminopyridine (4-AP) on the potassium currents in the node of Ranvier in myelinated nerve fibres was investigated with the voltage-clamp technique. The potential and time dependence of the currents in solutions with a high potassium concentration (114.5 mM) were studied. The block of the tail current was found to be less than that of the corresponding current during a potential step. Also, the time-course of the tail current was modified. In order to explain these findings, kinetic models of the 4-AP action were constructed and analysed numerically. A simple four-state model, in which 4-AP interacts only with open channels and where the binding is diphasically potential dependent, was found to account for the effects.

4-Aminopyridine↗
PubMed1988

Morphine activates calcium channels in cloned mouse neuroblastoma cell lines.

Membrane effects of morphine on cloned neuroblastoma cells (strains NG108-CC15 and N1E-115), were studied using intracellular recording and ion flux techniques. Morphine (10 microM) induced a depolarization that was affected by changes in the concentration of calcium, but not in sodium. Further, morphine induced an uptake of 45Ca2+ which was blocked by naloxone (1 microM). The simplest explanation for the findings is that morphine activates calcium channels via mu-receptors.

Animals↗
PubMed1987

Muscarinic receptors activate calcium channels and calcium dependent potassium channels in NlE-115 neuroblastoma cells.

Responses of NlE-115 neuroblastoma cells to application of carbachol were studied using intracellular recording techniques. Activation of muscarinic cholinergic receptors by carbachol resulted in a depolarization of the cells. The response was blocked by pirenzepine (1 microM) and by CoCl2 (5 mM), verapamil (10 microM) and gallopamil (10 microM), and prolonged by quinine (5 mM). It is suggested that muscarinic receptors increase the membrane calcium permeability, and that the influx of calcium activates calcium dependent potassium channels.

Animals↗
PubMed1986

The mechanism of action of ketamine on the myelinated nerve membrane.

Ketamine is an intravenous anaesthetic that has been reported to react with a number of synaptic and non-synaptic receptors at both the spinal and supraspinal level. The present investigation was undertaken to analyse the effects of ketamine on the myelinated axon under voltage clamp conditions. Both sodium and potassium channels were affected. The effect may be described as mainly a reduction of the permeability constants. No effect on inactivation was observed. The effects were described by a first order binding to receptors within the ion channels that may be identical with the receptors for other anaesthetics. It was concluded from experiments with naloxone that no opiate receptors were involved in the axonal ketamine effects.

Animals↗
PubMed1986

Ionic channels in the node of Ranvier are not modulated by cyclic adenosine monophosphate.

The effect of a cyclic adenosine monophosphate (cAMP) analogue on myelinated axons was studied. The lipophilic dibutyryl cAMP (dbcAMP) was applied to isolated frog axons under voltage clamp conditions. No effect on the ionic currents was observed for either external or internal application of dbcAMP. Nor was any effect of the phosphodiesterase inhibitor theophylline found. These results suggest that cAMP does not play an essential role for nerve impulse conduction in axons. This conclusion deviates from those of other studies.

Animals↗
PubMed1986

Non-muscarinic effects of scopolamine on N1E-115 neuroblastoma cells.

Membrane effects of scopolamine on N1E-115 neuroblastoma cells were studied using intracellular recording techniques. Scopolamine in concentrations of 50 nM-1 microM induced a depolarization together with a decreased cell input resistance. This response had a reversal potential at +10 to +20 mV in a medium with normal sodium concentration (146.5 mM), and a reversal potential around -10 mV when the sodium concentration in the medium was lowered to 80 mM. The scopolamine-induced depolarization could not be blocked by carbachol (100 microM), and had a reversal potential at +10 to +20 mV. The simplest explanation of the results obtained is that scopolamine increases the membrane permeability for sodium and potassium, in a manner which is not related to muscarinic cholinergic receptors.

Animals↗
PubMed1985

Ionic mechanisms of 3 types of functionally different neurons in the lamprey spinal cord.

Action potentials and afterpotentials were compared in giant interneurons, sensory dorsal cells and large intraspinal axons in the lamprey spinal cord. Afterpotentials of giant interneurons and dorsal cells consisted of two hyperpolarizing phases, an early and a late one, which were separated by a delayed depolarization. The afterpotentials of axons had a single hyperpolarizing phase also followed by a delayed depolarization. Tetraethyl ammonium chloride (TEA+) eliminated the early phase of the afterhyperpolarization in giant interneurons, only partially reduced the early phase in dorsal cells and did not affect the single phase of axons. The delayed depolarization of dorsal cells was attenuated by TEA+ but in axons it was unaltered. The heavy metal ions Mn2+ and Co2+ (2 mM) eliminated the late phase in giant interneurons but did not reduce the late phase in dorsal cells. The delayed depolarization remained in both types of cell in the presence of these ions. Action potentials of giant interneurons and dorsal cells, but not those of axons, were broadened by TEA+. The TEA-prolonged action potentials were narrowed by Mn2+ applied in combination with TEA+. The afterhyperpolarizations of all 3 cells were reduced by injection of negative current and enhanced by positive current. Repetitive stimulation resulted in summation of the afterhyperpolarization in giant interneurons and dorsal cells. The results suggest that different sets of potassium channels are responsible for the afterhyperpolarizations in each type of cell. In giant interneurons fast channels which are sensitive to TEA+ may underlie the early phase and slow channels activated by calcium entry may underlie the slow phase. The early phase of dorsal cells may be caused by two types of fast channel, one similar to that in giant interneurons and another less sensitive to external TEA+. This latter type may also cause the afterhyperpolarization in axons. Although calcium channels appear to contribute to the action potentials of giant interneurons and dorsal cells, the late phase of the latter neurons does not seem to be activated by calcium entry. The delayed depolarizations of the neurons appear to be due to an inward current which is not carried by calcium.

Action Potentials↗
PubMed1985

The effect of crown ethers on ionic currents in myelinated nerve fibres from Xenopus laevis.

The effect of several crown ethers on the currents at the node of Ranvier was studied. At differing potencies they caused a time- and potential-dependent inactivation of potassium permeability and a time- and potential-independent decrease in sodium permeability. The relative effect on potassium and sodium systems varied and was not directly related to their ionophoric properties. A computer analysis indicated that the induced inactivation was dependent on the normal potassium activation mechanism.

Action Potentials↗
PubMed1982

Inactivation of the potassium transport system of myelinated nerve in the presence of a cyclic ionophore.

A potassium carrying ionophore dicyclohexano-18-crown-6 was found to affect the specific ionic currents in the node of Ranvier. Its presence caused an inactivation of the potassium permeability mechanism and a decrease of the sodium permeability. The rate of inactivation of the potassium permeability depended on crown ether concentration, on membrane potential and on temperature. At large concentrations, the rate of inactivation was of the same order of size as the normal rate of activation. The recovery from the inactivated state was slow, it took a few seconds, and recovery time depended on holding potential. The inactivation was caused by potential steps in positive direction. The uncomplexed crown ether is uncharged and does not move due to a potential gradient. The mechanism by which the crown ether makes the inactivation potential dependent remains obscure. A few other ionophores were tested but they did not affect the membrane currents.

Animals↗
PubMed1981

A barbiturate-induced potassium permeability increase in the myelinated nerve membrane.

Effects of the highly lipid soluble barbiturates methohexital and thiopental on potential clamped myelinated nerve fibres were analyzed. Both were found to affect the potassium as well as sodium transport system. The methohexital effect on the potassium system was complex. At low potential values it reduced the permeability, while at high values it increased the permeability as well as slowed down the kinetics. It antagonized the rectification of IK at high potential values caused by increased axoplasmic [Na+]. The effect may be described as a combination of a decreased permeability constant (PK) and a methohexital induced potassium permeability with a potential and time dependence different to the ordinary potassium system. Thiopental reduced PK only. The effect on the sodium system was similar for the studied barbiturates and similar to that described for other barbiturates: a decrease of the permeability constant (PNa) and a shift of the h infinity-U relation in negative direction along the potential axis.

Action Potentials↗
PubMed1980

Effects of rubidium, caesium, strontium, barium and lanthanum on ionic currents in myelinated nerve fibres from Xenopus laevis.

A comparative analysis of the effects of externally applied Rb+, Cs+, Ba2+ and La3+ on myelinated fibres under potential clamp conditions was made. The ions Cs+, Ba2+ and La3+ (belonging to groups 1a, 2a and 3a of period 6 in the periodic system) were found to affect the K system in specific ways. Ba2+ and La3+ reduced the outward K+ current associated with positive potential steps; the effect of La3+ being larger than that of Ba2+. The effect of Ba2+ depended on the K+ concentration. Cs+, Ba2+ and La3+ reduced the inward K+ tail current at repolarisation in solutions with high K+ concentration. Cs+ and Ba2+ caused a rectification of the K+ current, i.e. they reduced the inward tail current proportionally more than the outward steady state current. The effect of Ba2+ could not be described as a simple reduction of the permeability constant PK. Rb+ was found to affect the time course of the K system by increasing the rate constant beta n. Sr2+, Ba2+ and La3+ reduced the permeability constant PNa. These ions also shifted potential dependent parameters in general along the potential axis. The effect of La3+ was larger than that of Sr2+ and Ba2+. Cs+, Ba2+ and La3+ reduced the p-current, Ba2+ and La3+ the leak conductance.

Action Potentials↗
PubMed1980

Effects of some heavy metal ions on the ionic currents of myelinated fibres from Xenopus laevis.

1. The effect of the heavy metal ions Mn2+, Co2+, Ni2+, Cu2+, Zn2+, Cd2+ and Hg2+ on permeability parameters of the nerve membrane was investigated. The ions were applied externally to single myelinated fibres of Xenopus laevis. The ionic currents, associated with potential steps were measured and analysed. 2. Zn2+ reversibly slowed down the kinetics of the K system. The effect at large potential steps was described as an increase of tau n. 3.4 mM-Zn2+ increased tau n about three times. 3. Ni2+ and Cu2+ also reversibly increased tau n in a similar way. The effect was larger than that of Zn2+. The other period 4 ions tested did not affect tau n markedly. Nor did the group 2b ion Cd2+. 4. The relative efficiency of the different ions agreed well with their tendency to form complexes with certain ligands. The effect was not a simple function of affinity for sulphydryl groups. 5. All the studied ions decreased PNa. The decrease was reversible except for that caused by Hg2+. Cu2+ caused the largest reversible effect. Hg2+ irreversibly decreased PNa at low concentrations (1-10 microM). 6. All ions studied shifted the Na activation curve in a positive direction along the potential axis. The effect was reversible except for that caused by Hg2+. The largest reversible shift was caused by Cu2+. 7. The relative efficiency of the different ions on the parameters studied in Xenopus axons showed great similarity to the corresponding efficiency on axons from other species, although some differences were noted.

Animals↗
PubMed1976

The effects of neuraminidase and protamine chloride on potential clamp parameters of the node of Ranvier (Xenopus laevis).

The effects of neuraminidase and protamine chloride on the ionic currents associated with step changes in membrane potential were studied. Neuraminidase (a hydrolase which cleaves glycosidically bound sialic acid) had negligible effects on the permeability properties. The polycation protamine chloride decreased the sodium as well as the potassium currents. The sodium equilibrium potential decreased during the experiments which indicates a gain in internal sodium concentration. The analysis showed that the effects on the currents were caused by a decrease of the specific permeability changes. No shift along the potential axis of the potential dependent parameters was observed.

Action Potentials↗