scholarly journals Grayanotoxin, veratrine, and tetrodotoxin-sensitive sodium pathways in the Schwann cell membrane of squid nerve fibers.

1976 ◽  
Vol 67 (3) ◽  
pp. 369-380 ◽  
Author(s):  
J Villegas ◽  
C Sevcik ◽  
F V Barnola ◽  
R Villegas

The actions of grayanotoxin I, veratrine, and tetrodotoxin on the membrane potential of the Schwann cell were studied in the giant nerve fiber of the squid Sepioteuthis sepioidea. Schwann cells of intact nerve fibers and Schwann cells attached to axons cut lengthwise over several millimeters were utilized. The axon membrane potential in the intact nerve fibers was also monitored. The effects of grayanotoxin I and veratrine on the membrane potential of the Schwann cell were found to be similar to those they produce on the resting membrane potential of the giant axon. Thus, grayanotoxin I (1-30 muM) and veratrine (5-50 mug-jl-1), externally applied to the intact nerve fiber or to axon-free nerve fiber sheaths, produce a Schwann cell depolarization which can be reversed by decreasing the external sodium concentration or by external application of tetrodotoxin. The magnitude of these membrane potential changes is related to the concentrations of the drugs in the external medium. These results indicate the existence of sodium pathways in the electrically unexcitable Schwann cell membrane of S. sepioidea, which can be opened up by grayanotoxin I and veratrine, and afterwards are blocked by tetrodotoxin. The sodium pathways of the Schwann cell membrane appear to be different from those of the axolemma which show a voltage-dependent conductance.

1971 ◽  
Vol 58 (1) ◽  
pp. 54-70 ◽  
Author(s):  
Toshio Narahashi ◽  
Edson X. Albuquerque ◽  
Takehiko Deguchi

The effects of batrachotoxin (BTX) on the membrane potential and conductances of squid giant axons have been studied by means of intracellular microelectrode recording, internal perfusion, and voltage clamp techniques. BTX (550–1100 nM) caused a marked and irreversible depolarization of the nerve membrane, the membrane potential being eventually reversed in polarity by as much as 15 mv. The depolarization progressed more rapidly with internal application than with external application of BTX to the axon. External application of tetrodotoxin (1000 nM) completely restored the BTX depolarization. Removal or drastic reduction of external sodium caused a hyperpolarization of the BTX-poisoned membrane. However, no change in the resting membrane potential occurred when BTX was applied in the absence of sodium ions in both external and internal phases. These observations demonstrate that BTX specifically increases the resting sodium permeability of the squid axon membrane. Despite such an increase in resting sodium permeability, the BTX-poisoned membrane was still capable of undergoing a large sodium permeability increase of normal magnitude upon depolarizing stimulation provided that the membrane potential was brought back to the original or higher level. The possibility that a single sodium channel is operative for both the resting sodium, permeability and the sodium permeability increase upon stimulation is discussed.


1992 ◽  
Vol 173 (1) ◽  
pp. 251-260
Author(s):  
P D Evans ◽  
V Reale ◽  
R M Merzon ◽  
J Villegas

The glutamate uptake blocker p-chloromercuriphenylsulphonic acid (PCMS) (100 mumol l-1) does not block any of the membrane potential changes induced by the application of L-glutamate to the adaxonal Schwann cells of the giant axon of the tropical squid Sepioteuthis sepioidea. This indicates that these potential changes are not due to the activation of an electrogenic glutamate uptake system and supports the idea that they are due to the activation of specific glutamate receptors. The presence of PCMS (100 mumol l-1) reduces the activity of the glutamate uptake system sufficiently for the extracellular level of axonally released glutamate to exceed the threshold for the activation of the NMDA-type glutamate receptors in this preparation.


1976 ◽  
Vol 69 (1) ◽  
pp. 19-28 ◽  
Author(s):  
GM Villegas ◽  
J Villegas

Giant nerve fibers of squid Sepioteuthis sepiodea were incubated for 10 min in artificial sea water (ASW) under control conditions, in the absence of various ions, and in the presence of cardiac glycosides. The nerve fibers were fixed in OsO(4) and embedded in Epon, and structural complexes along the axolemma were studied. These complexes consist of a portion of axolemma exhibiting a three-layered substructure, an undercoating of a dense material (approximately 0.1μm in length and approximately 70-170 A in thickness), and a narrowing to disappearance of the axon-Schwann cell interspace. In the controls, the incidence of complexes per 1,000μm of axon perimeter was about 137. This number decreased to 10-25 percent when magnesium was not present in the incubating media, whatever the calcium concentration (88, 44, or 0 mM). In the presence of magnesium, the number and structural features of the complexes were preserved, though the number decreased to 65 percent when high calcium was simultaneously present. The complexes were also modified and decreased to 26-32 percent by incubating the nerves in solutions having low concentrations of sodium and potassium. The adding of 10(-5) M ouabain or strophanthoside to normal ASW incubating solution decreased them to 20-40 percent. Due to their sensitivity to changes in external ionic concentrations and to the presence of cardiac glycosides, the complexes are proposed to represent the structural correlate of specialized sites for active ion transport, although other factors may be involved.


1999 ◽  
Vol 202 (4) ◽  
pp. 417-428
Author(s):  
P.D. Evans ◽  
V. Reale ◽  
R.M. Merzon ◽  
J. Villegas

A vasoactive intestinal peptide (VIP)-like peptide is released by axonal stimulation in the giant axon-Schwann cell preparation from the tropical squid Sepioteuthis sepioidea. It is also released by direct application of l-glutamate, the giant axon-Schwann cell signalling molecule in this preparation. The release of the peptide parallels the release of acetylcholine from the Schwann cells themselves in this preparation in a number of different ways. The release of both acetylcholine and the VIP-like peptide have the same threshold (between 2×10(−10) and 5×10(−10)mol l-1) for l-glutamate application and the same recovery time after inhibition of release by exposure of the preparation to a prolonged pulse of l-glutamate. A prolonged l-glutamate pulse of 10(−8)mol l-1 releases both substances for as long as the pulse is applied to the preparation, whereas a prolonged pulse of 10(−9)mol l-1 l-glutamate releases acetylcholine in the same way but releases the VIP-like peptide only transiently. The VIP-like peptide is likely to be co-released with acetylcholine from the Schwann cells.


1965 ◽  
Vol 208 (4) ◽  
pp. 720-723 ◽  
Author(s):  
Gordon M. Schoepfle ◽  
Eliska Atkins ◽  
Larry A. Schafer

Under conditions of continuous fluid exchange at a pH 7.55, a 10-min exposure of Xenopus sciatic single nerve fibers to iodoacetate results in eventual decline in the maximum rate of change of membrane potential, even after a delay of an hour or more during which no changes are apparent. This delayed effect is obtained over an iodoacetate concentration range of 0.1–20.0 mm sodium iodoacetate. Neither the resting membrane potential nor the maximal limiting response obtained during hyperpolarization are affected at a time when iodoacetate has appreciably depressed the spike in the nonpolarized fiber. These findings are taken to indicate that iodoacetate blocks a chain of reactions at a link remote from the process directly concerned with maintenance of the resting level of the sodium conductance. Neither lactate nor pyruvate can be relied on to bring about recovery from the iodoacetate depression.


1967 ◽  
Vol 50 (7) ◽  
pp. 1929-1953 ◽  
Author(s):  
Alfred Strickholm ◽  
B. Gunnar Wallin

The changes in membrane potential of isolated, single crayfish giant axons following rapid shifts in external ion concentrations have been studied. At normal resting potential the immediate change in membrane potential after a variation in external potassium concentration is quite marked compared to the effect of an equivalent chloride change. If the membrane is depolarized by a maintained potassium elevation, the immediate potential change due to a chloride variation becomes comparable to that of an equivalent potassium change. There is no appreciable effect on membrane potential when external sodium is varied, at normal or at a depolarized membrane potential. Starting from the constant field equation, expressions for the permeability ratios PCl/PK, PNa/PK, and for intracellular potassium and chloride concentrations are derived. At normal resting membrane potential, PCl/PK is 0.13 but at a membrane potential of -53 mv (external potassium level increased about five times) it is 0.85. The intracellular concentrations of potassium and chloride are estimated to be 233 and 34 mM, respectively, and it is pointed out that this is not compatible with ions distributed in a Nernst equilibrium across the membrane. It is also stressed that the information given by a plot of membrane potential vs. the logarithm of external potassium concentrations is very limited and rests upon several important assumptions.


1961 ◽  
Vol 44 (6) ◽  
pp. 1055-1057 ◽  
Author(s):  
Kenneth S. Cole

The membrane current density, Im, in the squid giant axon has been calculated from the measured external current applied to the axon, Io, by the equation See PDF for Equation where Vm is the membrane potential under the current electrode and r1 and r2 are the external and internal longitudinal resistances. The original derivation of this equation included in one step an assumption of a linear relation between Im and Vm. It is shown that the same equation can be obtained without this restricting assumption.


1964 ◽  
Vol 47 (4) ◽  
pp. 719-733 ◽  
Author(s):  
W. H. Herzog ◽  
R. M. Feibel ◽  
S. H. Bryant

In the giant axon of Loligo pealii, "aconitine potent" Merck added to the bath (10-7 to 1.25 x 10-6 gm/ml) (a) had no effect on resting membrane potential, membrane resistance and rectification, membrane response to subthreshold currents, critical depolarization, or action potential, but (b) on repetitive stimulation produced oscillations of membrane potential after the spike, depolarization, and decrease of membrane resistance. The effect sums with successive action potentials; it increases with concentration of aconitine, time of exposure, and frequency of stimulation. When the oscillations are large enough and the membrane potential is 51.6 ± SD 1.5 mv a burst of self-sustained activity begins; it usually lasts 20 to 70 sec. and at its end the membrane potential is 41.5 ± SD 1.9 mv. Repolarization occurs with a time constant of 2.5 to 11.1 min. Substitution of choline for external sodium after a burst hyperpolarizes the membrane to -70 mv, and return to normal external sodium depolarizes again beyond the resting membrane potential. The effect of aconitine on the membrane is attributed to an increase of sodium and potassium or chloride conductances following the action potential.


1980 ◽  
Vol 209 (1176) ◽  
pp. 441-446 ◽  

Previous studies by a number of workers have shown that the axon membrane in normal mature myelinated fibres is highly differentiated, with the nodal axolemma exhibiting characteristics different to those of the internodal axolemma. However, the development of this axolemmal heterogeneity has not been previously explored. In the present study we used cytochemical methods to examine the development of nodal axolemma during the differentiation of myelinated fibres in rat spinal roots. The staining properties characteristic of normal nodal membrane appear in the axon, at gaps between Schwann cells, before the develop­ment of mature compact myelin or well defined paranodal axon-Schwann cell specializations close to the region of nodal axolemmal differentiation. These results are consistent with the hypothesis that the axon membrane differentiates into nodal and internodal regions before, or early in the process of, myelination, and suggest that the differentiation of the axon membrane may provide a signal demarcating the region to be covered by the myelin-forming cell.


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