scholarly journals Peptidergic modulation of the membrane potential of the Schwann cell of the squid giant nerve fibre.

1986 ◽  
Vol 379 (1) ◽  
pp. 61-82 ◽  
Author(s):  
P D Evans ◽  
V Reale ◽  
J Villegas
Keyword(s):  
Membrane Potential ◽  
Schwann Cell ◽  
Nerve Fibre

Substance P modulation of the membrane potential of the Schwann cell of the squid giant nerve fibre

Glia ◽  
1990 ◽  
Vol 3 (5) ◽  
pp. 393-404 ◽  
Author(s):  
Peter D. Evans ◽  
Vincenzina Reale ◽  
Rosa Maria Merzon ◽  
Jorge Villegas
Keyword(s):  
Membrane Potential ◽  
Substance P ◽  
Schwann Cell ◽  
Nerve Fibre

scholarly journals N-methyl-D-aspartate (NMDA) and non-NMDA (metabotropic) type glutamate receptors modulate the membrane potential of the Schwann cell of the squid giant nerve fibre.

1992 ◽  
Vol 173 (1) ◽  
pp. 229-249 ◽  
Author(s):  
P D Evans ◽  
V Reale ◽  
R M Merzon ◽  
J Villegas
Keyword(s):  
Amino Acids ◽  
Membrane Potential ◽  
Schwann Cell ◽  
Glutamate Receptors ◽  
Nerve Fibre ◽  
Excitatory Amino Acids ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate ◽  
Type Receptor ◽  
Lasting Change

L-Glutamate application can produce three different responses in the membrane potential of the Schwann cell of the tropical squid, Sepioteuthis sepioidea, which appear to be mediated by three pharmacologically distinct classes of receptor. A class of non-NMDA-type receptors, with some similarities to metabotropic glutamate receptors, mediates the development of a rapid and long-lasting hyperpolarization. Two pharmacologically distinct classes of NMDA-type receptor are present. One mediates the development of a slow depolarization accompanied by a long-lasting change in responsiveness of the Schwann cell. The second produces rapid depolarizing responses during the period of this changed responsiveness. All three types of receptor can be activated by dipeptides containing excitatory amino acids.

scholarly journals The action of vasoactive intestinal peptide antagonists on peptidergic modulation of the squid Schwann cell

1988 ◽  
Vol 138 (1) ◽  
pp. 259-269 ◽  
Author(s):  
P. D. Evans ◽  
J. Villegas
Keyword(s):  
Membrane Potential ◽  
Substance P ◽  
Schwann Cell ◽  
Vasoactive Intestinal Peptide ◽  
Nerve Fibre ◽  
Giant Axon ◽  
Potency Ratio ◽  
Vip Receptors ◽  
Exogenous Application

1. The effects of two specific antagonists of vasoactive intestinal peptide (VIP) receptors were investigated on the VIP-induced hyperpolarization of the membrane potential of the Schwann cell of the giant nerve fibre of the tropical squid. 2. Both (pCl-D-Phe6,Leu17)VIP and (N-Ac-Tyr1,D-Phe2)-GRF(1–29)amide competitively and reversibly blocked the effects of VIP in this preparation with the former compound being more potent than the latter. 3. The blocking actions of both antagonists were specific for the responses of this preparation to VIP. They did not block the actions of carbachol, DL-octopamine or substance P. 4. Both antagonists also reduced the effectiveness of an endogenous VIP-like component in the normal hyperpolarizing action of giant axon activity on the membrane potential of the Schwann cell, with the same potency ratio as for their actions on the effects induced by the exogenous application of VIP.

Axon/Schwann-cell relationships in the giant nerve fibre of the squid

1981 ◽  
Vol 95 (1) ◽  
pp. 135-151
Author(s):  
J. Villegas
Keyword(s):  
Membrane Potential ◽  
Schwann Cell ◽  
Nerve Fibre ◽  
Acetylcholine Receptors ◽  
Acetylcholinesterase Activity ◽  
Feedback Mechanism ◽  
External Application ◽  
Cell Responses ◽  
Acetylcholinesterase Enzyme ◽  
Acetylcholine Concentration

This communication summarizes the experimental evidence obtained in the giant nerve fibre of the tropical squid Sepioteuthis sepioidea, on the nature of the mechanism responsible for the long-lasting effects of axonal excitation on the membrane potential of the Schwann cell. In these nerve fibres the propagation of a train of nerve impulses by the axon is followed by a prolonged hyperpolarization of the Schwann cell which can be reproduced, or modified, by the external application of cholinergic compounds. The presence and exact localization of the different components of the acetylcholine system directly involved in such Schwann-cell responses was detected by means of pharmacological, histochemical and chemical procedures. Thus, the results of the experiments herein discussed revealed that, under physiological conditions: the Schwann cell is able to synthesize, store and release acetylcholine; and that it has acetylcholine receptors of the nicotinic type, and acetylcholinesterase enzyme activity in its plasma membrane. On the other hand, the axon has low acetyltransferase activity and acetylcholine concentration in its axoplasm, and a high acetylcholinesterase activity in its axolemma. It was also found that acetylcholine hyperpolarizes the Schwann cell by increasing its relative permeability to the potassium ion. The distribution pattern of the acetylcholine system indicates that it operates as a feedback mechanism for the regulation of the Schwann-cell membrane potential and ionic permeability following axonal excitation.

scholarly journals The effect of a glutamate uptake inhibitor on axon-Schwann cell signalling in the squid giant nerve fibre.

1992 ◽  
Vol 173 (1) ◽  
pp. 251-260
Author(s):  
P D Evans ◽  
V Reale ◽  
R M Merzon ◽  
J Villegas
Keyword(s):  
Membrane Potential ◽  
Schwann Cell ◽  
Glutamate Receptors ◽  
Schwann Cells ◽  
Nerve Fibre ◽  
Glutamate Uptake ◽  
Cell Signalling ◽  
Giant Axon ◽  
Uptake System ◽  
Extracellular Level

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.

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
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Schwann Cell ◽  
Nerve Fiber ◽  
Schwann Cells ◽  
Giant Axon ◽  
Nerve Fibers ◽  
Resting Membrane Potential ◽  
External Application ◽  
Axon Membrane

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.

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