scholarly journals Optical measurement of conduction in single demyelinated axons.

1990 ◽  
Vol 95 (5) ◽  
pp. 867-889 ◽  
Author(s):  
P Shrager ◽  
C T Rubinstein
Keyword(s):  
Schwann Cells ◽  
Action Potentials ◽  
Spontaneous Recovery ◽  
Demyelinating Disease ◽  
Optical Measurement ◽  
Recovery Of Function ◽  
Na Channels ◽  
Cable Properties ◽  
Probability Of Success ◽  
Voltage Dependent

Demyelination was initiated in Xenopus sciatic nerves by an intraneural injection of lysolecithin over a 2-3-mm region. During the next week macrophages and Schwann cells removed all remaining damaged myelin by phagocytosis. Proliferating Schwann cells then began to remyelinate the axons, with the first few lamellae appearing 13 d after surgery. Action potentials were recorded optically through the use of a potential-sensitive dye. Signals could be detected both at normal nodes of Ranvier and within demyelinated segments. Before remyelination, conduction through the lesion occurred in only a small fraction of the fibers. However, in these particular cases we could demonstrate continuous (nonsaltatory) conduction at very low velocities over long (greater than one internode) lengths of demyelinated axons. We have previously found through loose patch clamp experiments that the internodal axolemma contains voltage-dependent Na+ channels at a density approximately 4% of that at the nodes. These channels alone, however, are insufficient for successful conduction past the transition point between myelinated and demyelinated regions. Small improvements in the passive cable properties of the axon, adequate for propagation at this site, can be realized through the close apposition of macrophages and Schwann cells. As the initial lamellae of myelin appear, the probability of success at the transition zone increases rapidly, though the conduction velocity through the demyelinated segment is not appreciably changed. A detailed computational model is used to test the relative roles of the internodal Na+ channels and the new extracellular layer. The results suggest a possible mechanism that may contribute to the spontaneous recovery of function often seen in demyelinating disease.

Inward currents underlying action potentials in rat adrenal chromaffin cells

1996 ◽  
Vol 76 (2) ◽  
pp. 1195-1211 ◽  
Author(s):  
B. Hollins ◽  
S. R. Ikeda
Keyword(s):  
Ion Channels ◽  
Voltage Clamp ◽  
Action Potentials ◽  
Chromaffin Cells ◽  
Na Channels ◽  
Adrenal Chromaffin Cells ◽  
Voltage Dependent ◽  
Slope Factor ◽  
Inward Currents ◽  
Adrenal Chromaffin

1. Current- and voltage-clamp studies were conducted on isolated rat adrenal chromaffin cells to identify the voltage-dependent ion channels mediating inward currents. 2. Mean resting membrane potential of the isolated cells was -62 +/- 3 (SE) mV. Evoked action potentials were both Na+ and Ca2+ based, and whole cell voltage-clamp studies in normal saline revealed an inward-rectifier-type current. 3. Na+ channels were studied in isolation and showed a half-inactivation of -60 +/- 2 mV with a slope factor of -6 mV and a half-activation of -26.8 +/- 2 mV with a slope factor of 6.5 +/- 0.7 mV. 4. Isolated Ca2+ currents, elicited in 10 mM external Ca2+, revealed a T-type current in a subset of cells. Ca2+ currents were sensitive to both N- and L-type channel antagonists, and blockade of the current by the L-type channel antagonist nimodipine and the N-type channel antagonist omega-conotoxin GVIA revealed a third Ca2+-current component that was unaffected by the P-type channel antagonist omega-agatoxin IVA. 5. Ca2+ currents were facilitated 5-20% by a depolarizing prepulse, and facilitation was completely blocked by nimodipine. The effects of the dihydropyridine L-type channel agonist, (+)202-791 and depolarizing prepulses on the currents were additive. 6. The results of this study show that the properties of voltage-dependent ion channels in rat chromaffin cells differ from those reported in their counterparts in bovine chromaffin cells. Na+ channels differ in activation and inactivation properties and Ca2+ channels differ in activation, sensitivity to antagonists, and the magnitude of voltage-dependent facilitation.

scholarly journals A native prokaryotic voltage-dependent calcium channel with a novel selectivity filter sequence

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Takushi Shimomura ◽  
Yoshiki Yonekawa ◽  
Hitoshi Nagura ◽  
Michihiro Tateyama ◽  
Yoshinori Fujiyoshi ◽  
...  
Keyword(s):  
Action Potentials ◽  
Negative Charge ◽  
Selectivity Filter ◽  
Na Channels ◽  
Glycine Residue ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent ◽  
Living Organisms ◽  
Insight Into ◽  
Ca2 Channels

Voltage-dependent Ca2+ channels (Cavs) are indispensable for coupling action potentials with Ca2+ signaling in living organisms. The structure of Cavs is similar to that of voltage-dependent Na+ channels (Navs). It is known that prokaryotic Navs can obtain Ca2+ selectivity by negative charge mutations of the selectivity filter, but native prokaryotic Cavs had not yet been identified. We report the first identification of a native prokaryotic Cav, CavMr, whose selectivity filter contains a smaller number of negatively charged residues than that of artificial prokaryotic Cavs. A relative mutant whose selectivity filter was replaced with that of CavMr exhibits high Ca2+ selectivity. Mutational analyses revealed that the glycine residue of the CavMr selectivity filter is a determinant for Ca2+ selectivity. This glycine residue is well conserved among subdomains I and III of eukaryotic Cavs. These findings provide new insight into the Ca2+ selectivity mechanism that is conserved from prokaryotes to eukaryotes.

scholarly journals Biology of the repair of central nervous system demyelinated lesions: an appraisal

1996 ◽  
Vol 54 (2) ◽  
pp. 331-334 ◽  
Author(s):  
L. A. V Peireira ◽  
M. A. Cruz-Höfling ◽  
M. S. J. Dertkigil ◽  
D. L. Graça
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cells ◽  
Demyelinating Disease ◽  
Experimental Models ◽  
Primitive Cell ◽  
Marked Influence ◽  
Myelin Sheaths ◽  
Human Material ◽  
The Central Nervous System

The integrity of myelin sheaths is maintained by oligodendrocytes and Schwann cells respectively in the central nervous system (CNS) and in the peripheral nervous system. The process of demyelination consisting of the withdrawal of myelin sheaths from their axons is a characteristic feature of multiple sclerosis, the most common human demyelinating disease. Many experimental models have been designed to study the biology of demyelination and remyelination (repair of the lost myelin) in the CNS, due to the difficulties in studying human material. In the ethidium bromide (an intercalating gliotoxic drug) model of demyelination, CNS remyelination may be carried out by surviving oligodendrocytes and/or by cells differentiated from the primitive cell lines or either by Schwann cells that invade the CNS. However, some factors such as the age of the experimental animals, intensity and time of exposure to the intercalating chemical and the topography of the lesions have marked influence on the repair of the tissue.

Outward current and repolarization in hypoxic rat myocardium

1983 ◽  
Vol 244 (3) ◽  
pp. H341-H350
Author(s):  
C. H. Conrad ◽  
R. G. Mark ◽  
O. H. Bing
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Outward Current ◽  
Iodoacetic Acid ◽  
Mechanical Activity ◽  
Potential Range ◽  
Papillary Muscles ◽  
Rat Myocardium ◽  
Cable Properties ◽  
Sucrose Gap

We studied the effects of brief periods (20-30 min) of hypoxia in the presence of 5 and 50 mM glucose and of glycolytic blockade (10(-4) M iodoacetic acid, IAA) on action potentials, membrane currents, and mechanical activity in rat ventricular papillary muscles using a single sucrose gap voltage-clamp technique. Steady-state outward current (iss) was determined at the end of a 500-ms clamp to the test potential following a 600-ms clamp to a holding potential of -50 mV. In the presence of 5 mM glucose, hypoxia resulted in a decrease in action potential duration (APD) and an increase in iss (on the order of 60% at 0 mV) over the potential range studied. The increase in iss did not appear to be due to an increase in leakage current or to a change in the cable properties of the preparation. Addition of 50 mM glucose prevented the change in both APD and iss with hypoxia. In addition, glycolytic blockade with IAA did not alter iss in the presence of oxygen. We conclude that an increase in iss appears to be a major factor in the abbreviation of rat ventricular action potential seen with hypoxia. Glycolysis appears to be a sufficient (with 50 mM glucose) but not necessary source of energy for the maintenance of normal iss.

Electrical Properties and Anion Permeability of Doubly Rectifying Junctions in the Leech Central Nervous System

1988 ◽  
Vol 137 (1) ◽  
pp. 1-11
Author(s):  
Susan E. Acklin
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
T Cell ◽  
Action Potentials ◽  
Sodium Pump ◽  
Current Flow ◽  
Cell Movement ◽  
Voltage Dependent ◽  
Electrical Connections

A study has been made of the electrical connections between touch sensory (T) neurones in the leech central nervous system (CNS) which display remarkable double rectification: depolarization spreads in both directions although hyperpolarization spreads poorly. Tests were made to determine whether this double rectification was a property of the junctions themselves or whether it resulted from changes in the length constants of processes intervening between the cell body and the junctions. Following trains of action potentials, T cells and their fine processes within the neuropile became hyperpolarized through the activity of an electrogenie sodium pump. When any T cell was hyperpolarized by 25 mV by repetitive stimulation, hyperpolarization failed to spread to the T cells to which it was electrically coupled. Further evidence for double rectification of junctions linking T cells was provided by experiments in which Cl− was injected electrophoretically. Cl− injection into one T cell caused inhibitory potentials recorded in it to become reversed. After a delay, Cl− spread to reverse IPSPs in the coupled T cell. Movement of Cl−, like current flow, was dependent on membrane potential. When the T cell into which Cl− was injected was kept hyperpolarized, Cl− failed to move into the adjacent T cell. Upon release of the hyperpolarization in the injected T cell, Cl− moved and reversed IPSPs in the coupled T cell. Together these results indicate that the gating properties of channels linking T cells are voltage-dependent, such that depolarization of either cell allows channels to open whereas hyperpolarization causes them to close.

Simulator for neural networks and action potentials: description and application

1994 ◽  
Vol 71 (1) ◽  
pp. 294-308 ◽  
Author(s):  
I. Ziv ◽  
D. A. Baxter ◽  
J. H. Byrne
Keyword(s):  
Neural Networks ◽  
Central Pattern Generator ◽  
Action Potentials ◽  
Modular Design ◽  
Second Messenger ◽  
Pattern Generator ◽  
Slow Inward Current ◽  
Synaptic Connections ◽  
Different Types ◽  
Voltage Dependent

1. We describe a simulator for neural networks and action potentials (SNNAP) that can simulate up to 30 neurons, each with up to 30 voltage-dependent conductances, 30 electrical synapses, and 30 multicomponent chemical synapses. Voltage-dependent conductances are described by Hodgkin-Huxley type equations, and the contributions of time-dependent synaptic conductances are described by second-order differential equations. The program also incorporates equations for simulating different types of neural modulation and synaptic plasticity. 2. Parameters, initial conditions, and output options for SNNAP are passed to the program through a number of modular ASCII files. These modules can be modified by commonly available text editors that use a conventional (i.e., character based) interface or by an editor incorporated into SNNAP that uses a graphical interface. The modular design facilitates the incorporation of existing modules into new simulations. Thus libraries can be developed of files describing distinctive cell types and files describing distinctive neural networks. 3. Several different types of neurons with distinct biophysical properties and firing properties were simulated by incorporating different combinations of voltage-dependent Na+, Ca2+, and K+ channels as well as Ca(2+)-activated and Ca(2+)-inactivated channels. Simulated cells included those that respond to depolarization with tonic firing, adaptive firing, or plateau potentials as well as endogenous pacemaker and bursting cells. 4. Several types of simple neural networks were simulated that included feed-forward excitatory and inhibitory chemical synaptic connections, a network of electrically coupled cells, and a network with feedback chemical synaptic connections that simulated rhythmic neural activity. In addition, with the use of the equations describing electrical coupling, current flow in a branched neuron with 18 compartments was simulated. 5. Enhancement of excitability and enhancement of transmitter release, produced by modulatory transmitters, were simulated by second-messenger-induced modulation of K+ currents. A depletion model for synaptic depression was also simulated. 6. We also attempted to simulate the features of a more complicated central pattern generator, inspired by the properties of neurons in the buccal ganglia of Aplysia. Dynamic changes in the activity of this central pattern generator were produced by a second-messenger-induced modulation of a slow inward current in one of the neurons.

Voltage-Dependent Properties of Dendrites That Eliminate Location-Dependent Variability of Synaptic Input

1999 ◽  
Vol 81 (2) ◽  
pp. 535-543 ◽  
Author(s):  
Erik P. Cook ◽  
Daniel Johnston
Keyword(s):  
Synaptic Input ◽  
Outward Current ◽  
Compartment Model ◽  
Inward Current ◽  
Voltage Gated ◽  
Cable Properties ◽  
Dendritic Membrane ◽  
Voltage Dependent ◽  
Dendritic Location ◽  
Voltage Gated Channels

Voltage-dependent properties of dendrites that eliminate location-dependent variability of synaptic input. We examined the hypothesis that voltage-dependent properties of dendrites allow for the accurate transfer of synaptic information to the soma independent of synapse location. This hypothesis is motivated by experimental evidence that dendrites contain a complex array of voltage-gated channels. How these channels affect synaptic integration is unknown. One hypothesized role for dendritic voltage-gated channels is to counteract passive cable properties, rendering all synapses electrotonically equidistant from the soma. With dendrites modeled as passive cables, the effect a synapse exerts at the soma depends on dendritic location (referred to as location-dependent variability of the synaptic input). In this theoretical study we used a simplified three-compartment model of a neuron to determine the dendritic voltage-dependent properties required for accurate transfer of synaptic information to the soma independent of synapse location. A dendrite that eliminates location-dependent variability requires three components: 1) a steady-state, voltage-dependent inward current that together with the passive leak current provides a net outward current and a zero slope conductance at depolarized potentials, 2) a fast, transient, inward current that compensates for dendritic membrane capacitance, and 3) both αamino-3-hydroxy-5-methyl-4-isoxazolepropionic acid– and N-methyl-d-aspartate–like synaptic conductances that together permit synapses to behave as ideal current sources. These components are consistent with the known properties of dendrites. In addition, these results indicate that a dendrite designed to eliminate location-dependent variability also actively back-propagates somatic action potentials.

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