Macromolecular structure of axon membrane and action potential conduction in myelin deficient and myelin deficient heterozygote rat optic nerves

Receptor-mediated calcium signaling in axons of mouse and rat optic nerves was examined by selectively staining the axonal population with a calcium indicator. Nicotine (1-50 μM) induced an axonal calcium elevation that was eliminated when calcium was removed from the bath, suggesting that nicotine induces calcium influx into axons. The nicotine response was blocked by d-tubocurarine and mecamylamine but not α-bungarotoxin, indicating the presence of calcium permeable, non-α7 nicotinic acetylcholine receptor (nAChR) subtype. Agonist efficacy order for eliciting the axonal nAChR calcium response was cytisine ∼ nicotine >> acetylcholine. The nicotine-mediated calcium response was attenuated during the process of normal myelination, decreasing by approximately 10-fold from P1 (premyelinated) to P30 (myelinated). Nicotine also caused a rapid reduction in the compound action potential in neonatal optic nerves, consistent with a shunting of the membrane after opening of the nonspecific cationic nicotinic channels. Voltagegated calcium channels contributed little to the axonal calcium elevation during nAChR activation. During repetitive stimulations, the compound action potential in neonatal mouse optic nerves underwent a gradual reduction in amplitude that could be partially prevented by d-tubocurarine, suggesting an activity-dependent release of acetylcholine that activates axonal AChRs. We conclude that mammalian optic nerve axons express nAChRs and suggest that these receptors are activated in an activity-dependent fashion during optic nerve development to modulate axon excitability and biology.

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Transplantation of glial cells enhances action potential conduction of amyelinated spinal cord axons in the myelin-deficient rat.

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.91.1.53 ◽

1994 ◽

Vol 91 (1) ◽

pp. 53-57 ◽

Cited By ~ 104

Author(s):

D. A. Utzschneider ◽

D. R. Archer ◽

J. D. Kocsis ◽

S. G. Waxman ◽

I. D. Duncan

Keyword(s):

Spinal Cord ◽

Action Potential ◽

Glial Cells ◽

Myelin Deficient

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The development of the transferrin—transferrin receptor system in relation to astrocytes, MBP and galactocerebroside in normal and myelin-deficient rat optic nerves

Developmental Brain Research ◽

10.1016/0165-3806(89)90029-1 ◽

1989 ◽

Vol 49 (2) ◽

pp. 281-293 ◽

Cited By ~ 45

Author(s):

Helen H. Lin ◽

James R. Connor

Keyword(s):

Transferrin Receptor ◽

Receptor System ◽

Optic Nerves ◽

Myelin Deficient

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Axon membrane skeleton effect on axonal membrane protein diffusion and action potential propagation

10.26226/morressier.5f5f8e69aa777f8ba5bd6146 ◽

2020 ◽

Author(s):

George Lykotrafitis

Keyword(s):

Membrane Protein ◽

Action Potential ◽

Membrane Skeleton ◽

Protein Diffusion ◽

Axonal Membrane ◽

Axon Membrane ◽

Action Potential Propagation

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Effects of Ethanol and Temperature on a Crab Motor Axon Action Potential: A Possible Mechanism for Peripheral Spike Generation

Journal of Experimental Biology ◽

10.1242/jeb.103.1.289 ◽

1983 ◽

Vol 103 (1) ◽

pp. 289-301 ◽

Cited By ~ 1

Author(s):

PHILIP J. STEPHENS ◽

PAUL A. FRASCELLA ◽

NORMAN MINDREBO

Keyword(s):

Action Potential ◽

Refractory Period ◽

Action Potentials ◽

Time Course ◽

Membrane Resistance ◽

Temperature Threshold ◽

Spike Generation ◽

Axon Membrane ◽

Potential Spike ◽

Low Threshold

1. In autotomized walking limbs of Pachygrapsus crassipes, microelectrode recordings of evoked action potentials were made in the meropodite from the E2 excitor axon to the bender muscle. 2. The action potential spike was followed by a depolarizing after-potential. Increases in temperature resulted in a decline in the amplitude and time course of the spike, and an increase in the amplitude of the after-potential. Low levels of ethanol or increased levels of calcium increased the size of the after-potential and decreased the temperature threshold for peripheral spike generation. 3. At high temperatures a single orthodromic E2 axon spike provoked the generation of additional impulses at the periphery, with an inter-spike interval of 2–3.5 ms. 4. The after-potential lasted longer than the refractory period following the spike. The axon membrane, therefore, was depolarized after the refractory period and this resulted in a period of low threshold for spike generation. Increases in temperature shortened the refractory period. 5. We suggest that additional spikes are generated at the periphery where the E2 axon diameter is decreased. The increased membrane resistance at these sites increases the size of the depolarizing after-potential. Therefore, if the depolarization following the refractory period is at or above threshold for firing, additional action potentials will be generated at the periphery.

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Axonal Adaptations to Osmotic and Ionic Stress in an Invertebrate Osmoconformer (Mercierella Enigmatica Fauvel): II. Effects of Ionic Dilution on the Resting and Action Potentials

Journal of Experimental Biology ◽

10.1242/jeb.76.1.205 ◽

1978 ◽

Vol 76 (1) ◽

pp. 205-219

Author(s):

J. A. BENSON ◽

J. E. TREHERNE

Keyword(s):

Action Potential ◽

Action Potentials ◽

Prolonged Exposure ◽

Giant Axon ◽

Sodium Concentration ◽

Ionic Concentration ◽

Osmotic Concentration ◽

Bathing Medium ◽

Axon Membrane ◽

Wide Range

The giant axon of this extreme euryhaline osmoconformer possess an unusual ability to produce action potentials of large amplitude over a wide range of ionic dilution when constant osmotic concentration is maintained by the addition of mannitol to the bathing medium. Ionic dilution under these circumstances causes a decline in the overshoot of the action potential (resulting largely from reduction in [Na+]0) and an appreciable axonal hyperpolarization (primarily as a result of decrease in [K+]0). This hyperpolarization tends to compensate for the reduction in the extent of the overshoot and so maintains the amplitude of the sodium-mediated action potentials during isosmotic dilution of the bathing medium. The axonal hyperpolarization also appears to reduce sodium inactivation so as to maintain a rapid rate of rise of the action potential despite drastic reduction in the ionic concentration of the bathing medium. Prolonged exposure to reduced ionic concentrations appears to induce a ouabain sensitive reduction in intracellular sodium concentration which increases the sodium gradient across the axon membrane during isosmotic dilution of the external medium.

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Ionic currents in giant motor axons of the jellyfish, Aglantha digitale

Journal of Neurophysiology ◽

10.1152/jn.1993.69.3.884 ◽

1993 ◽

Vol 69 (3) ◽

pp. 884-893 ◽

Cited By ~ 28

Author(s):

R. W. Meech ◽

G. O. Mackie

Keyword(s):

Action Potential ◽

Outward Current ◽

Inactivation Kinetics ◽

Motor Axons ◽

Bathing Medium ◽

Axon Membrane ◽

Inward Current ◽

Low Threshold Spike ◽

Low Threshold ◽

Attached Membrane

1. In the motor system of the jellyfish, Aglantha digitale, there are eight giant axons connected by chemical synapses to a muscle epithelium. The simplicity of this structure makes it possible to assess the contribution of different ion conductances in the axon membrane to the two forms of swimming that provide the behavioral output of the system. In situ recordings from large clusters of ion channels provide a means of studying these membrane conductances in isolation so that the features that permit them to perform their behavioral function may be identified. 2. In Aglantha motor axons, low-amplitude, low-threshold spikes are associated with slow swimming, whereas escape swimming depends on a higher-threshold, overshooting action potential. The action potential was abolished by a sodium-free (choline-containing) bathing medium but was resistant to tetrodotoxin (0.09 mM; 3 x 10(-5) g/ml). It was prolonged by tetraethylammonium (TEA) ions (50 mM) but little affected by changes in holding potential in the range of -51 to -82 mV. The low-threshold spikes were unaffected by sodium-free saline containing TEA (30 mM). They were inactivated by holding the membrane potential at -51 mV. Average axon resting potentials were -63 +/- 6 (SD) mV (n = 17). 3. Shortened axons studied with the two-electrode voltage-clamp technique had a transient inward current with a low threshold for activation (about -60 mV). The inward current was fully inactivated at -51 mV; it was present in sodium-free saline and abolished by Mg2+ (120 mM) just like the low-threshold spike. 4. Calcium-dependent low-threshold spikes and sodium action potentials coexist in the same axons but may be elicited separately because an outward current limits the peak of the low-threshold spike to a level below the threshold of the action potential (about -20 mV). 5. Analysis of ensemble currents showed that axon-attached membrane patches contained clusters of different voltage-dependent potassium channels. Three channel classes were distinguished by prepulse inactivation experiments. All three channels were found to inactivate, but they had different voltage-dependencies and different inactivation kinetics (fast, intermediate, or slow). Recovery from inactivation was slow in each case (time constant 2–10 s). 6. All axon-attached membrane patches were found to contain one or two of the three classes of potassium channel. Channels with intermediate kinetics were found less frequently and may have been present at lower density.(ABSTRACT TRUNCATED AT 400 WORDS)

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Contribution of sodium pump to resting potential of squid giant axon

AJP Cell Physiology ◽

10.1152/ajpcell.1978.235.1.c55 ◽

1978 ◽

Vol 235 (1) ◽

pp. C55-C62 ◽

Cited By ~ 17

Author(s):

P. de Weer ◽

D. Geduldig

Keyword(s):

Membrane Potential ◽

Action Potential ◽

Sodium Pump ◽

Membrane Conductance ◽

Giant Axon ◽

Membrane Depolarization ◽

Resting Potential ◽

Potassium Efflux ◽

Axon Membrane ◽

Potassium Permeability

The effect of the cardiotonic aglycone, strophanthidin, on sodium and potassium efflux, membrane potential, membrane conductance, potassium permeability, and the shape of the action potential of the giant axon of the squid, Loligo pealei, was examined. Strophanthidin depolarized the membrane to an extent determined by the intracellular sodium concentration, except in axons pretreated with cyanide, in which the effect is abolished. Cyanide itself hyperpolarized the axon membrane. Axons treated with strophanthidin appear to be better potassium electrodes, but this observation is fully accounted for by the stimulating effect of [K]o on an electrogenic sodium pump. The increase in potassium efflux produced by strophanthidin is also well accounted for by the observed membrane depolarization and the known dependence of potassium permeability on membrane potential (e-fold increase in efflux per 6.4 mV depolarization). Strophanthidin has no demonstrable effect on membrane conductance apart from that due to the observed depolarization. These findings support the view that cardiotonic steroids, at least in nerve, are specific inhibitors of the sodium pump, devoid of effects on permeability that might interfere with the study of electrogenic pumping. The alteration in the shape of the action potential after exposure to strophanthidin (deepening of the "underswing") suggests that the strophanthidin-induced membrane depolarization results from the inhibition of a true electrogenic pump, and not from ion redistributions in the vicinity of the membrane.

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