A comparison of the release of a vasoactive-intestinal-peptide-like peptide and acetylcholine in the giant axon-Schwann cell preparation of the tropical squid Sepioteuthis sepioidea

1999 ◽  
Vol 202 (4) ◽  
pp. 417-428
Author(s):  
P.D. Evans ◽  
V. Reale ◽  
R.M. Merzon ◽  
J. Villegas
Keyword(s):  
Schwann Cell ◽  
Vasoactive Intestinal Peptide ◽  
Schwann Cells ◽  
Recovery Time ◽  
Cell Signalling ◽  
Giant Axon ◽  
Direct Application ◽  
Cell Preparation ◽  
Signalling Molecule ◽  
Release Of Acetylcholine

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.

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.

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

1986 ◽  
Vol 121 (1) ◽  
pp. 421-443 ◽  
Author(s):  
V. Reale ◽  
P. D. Evans ◽  
J. Villegas
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Nerve Fibre ◽  
High Frequency ◽  
Cell Activity ◽  
Physiological Role ◽  
Giant Axon ◽  
Octopamine Receptors ◽  
Low Concentrations

The actions of octopamine on the Schwann cells of the giant nerve fibre of the tropical squid are described. The pharmacology of the receptors mediating the actions of octopamine has been investigated in terms of stereospecificity, amine specificity and interactions with a range of agonists and antagonists. The receptors are maximally activated by D(−)-octopamine and share many of the characteristics of OCTOPAMINE2 class receptors in other preparations. The octopamine receptors appear to mediate their actions by increasing the intracellular levels of cyclic AMP in the Schwann cells. Low concentrations of octopamine potentiate the actions of the nicotinic cholinergic activation system of the Schwann cells. The results are discussed in terms of the possible physiological role of octopamine in the modulation of Schwann cell activity during stressful conditions when the giant axon system is likely to be used at a high frequency to facilitate the escape response of the squid.

Three markers of adult non-myelin-forming Schwann cells, 217c(Ran-1), A5E3 and GFAP: development and regulation by neuron-Schwann cell interactions

Development ◽  
1990 ◽  
Vol 109 (1) ◽  
pp. 91-103 ◽  
Author(s):  
K.R. Jessen ◽  
L. Morgan ◽  
H.J. Stewart ◽  
R. Mirsky
Keyword(s):  
Sciatic Nerve ◽  
Schwann Cell ◽  
Schwann Cells ◽  
Cell Signalling ◽  
Surface Proteins ◽  
Developmental Changes ◽  
Rat Sciatic Nerve ◽  
Ngf Receptor ◽  
Cultured Schwann Cells ◽  
Do So

Immunohistochemical methods are used to investigate in detail the development and regulation of three proteins (217c(Ran-1), A5E3 and GFAP) specifically associated with adult non-myelin-forming Schwann cells in the rat sciatic nerve, from embryo day 15 to maturity. 217c(Ran-1), which is probably the NGF-receptor, and A5E3 are expressed by the majority of cells in the nerve at embryo day 15 and by essentially all cells at embryo day 18. GFAP first appears at embryo day 18; this is an intrinsically programmed developmental event which occurs in cultured Schwann cells even in the absence of serum. Postnatally, the expression of 217c(Ran-1), A5E3 and GFAP is suppressed in cells that form myelin but retained in non-myelin-forming Schwann cells. Mature myelin-forming cells nevertheless maintain the potential to express all three proteins but will only do so if removed from contact with myelinated axons. In neuron-free cultures Schwann cells express all three proteins. This work, together with our previous observations on N-CAM, shows that removal of a diverse set of surface proteins and a change in intermediate filament expression is one of the major consequences of axon to Schwann cell signalling during myelination in the rat sciatic nerve. Unlike myelin-forming cells, adult non-myelin-forming Schwann cells remain very similar to embryonic and newborn cells with respect to expression of surface proteins, in contrast to the previously established developmental changes that occur in their surface lipids.

Coupling between giant axon Schwann cells in the squid

1996 ◽  
Vol 263 (1370) ◽  
pp. 667-672 ◽  
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Sea Water ◽  
Electrical Coupling ◽  
Giant Axon ◽  
Membrane Resistance ◽  
Weakly Coupled ◽  
Length Constant ◽  
Spatial Buffering ◽  
Cell Sheath

The nature of dye and electrical coupling between Schwann cells from the the squid giant axon, determined with microelectrodes, is described. Dye coupling (sensitive to dissection in sea water containing Ca 2+ ) and electrical coupling exists between Schwann cells. The electrical length constant of the Schwann-cell sheath is 25 µm and 100 µm along the axon circumference and long axis respectively. Schwann-cell membrane resistance is ~ 500 Ω cm 2 (corrected for coupling between cells). The coupling ratio between cells is 1:0.3, and is reduced by 2 mm octanol (1:0.03) and increased by 2 mm Ba 2+ (1:0.45). We conclude that as Schwann cells are weakly coupled and have a relatively low membrane resistance they are unlikely to be involved in the spatial buffering of axonally released K + .

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.

Human Neurofibromas in Co-Culture with Mouse Neurons

1982 ◽  
Vol 40 ◽  
pp. 194-195
Author(s):  
R.L. Martuza ◽  
T. Liszczak ◽  
A. Okun ◽  
T-Y Wang
Keyword(s):  
Schwann Cell ◽  
Schwann Cells ◽  
Genetic Disorder ◽  
Cranial Nerves ◽  
Sympathetic Nerves ◽  
Acoustic Neuromas ◽  
Spinal Roots ◽  
Neural Crest Origin ◽  
Multiple Abnormalities ◽  
Other Neoplasms

Neurofibromatosis (NF) is an autosomal dominant genetic disorder with a prevalence of 1/3,000 births. The NF mutation causes multiple abnormalities of various cells of neural crest origin. Schwann cell tumors (neurofibromas, acoustic neuromas) are the most common feature of neurofibromatosis although meningiomas, gliomas, and other neoplasms may be seen. The schwann cell tumors commonly develop from the schwann cells associated with sensory or sympathetic nerves or their ganglia. Schwann cell tumors on ventral spinal roots or motor cranial nerves are much less common. Since the sensory neuron membrane is known to contain a mitogenic factor for schwann cells, we have postulated that neurofibromatosis may be due to an abnormal interaction between the nerve and the schwann cell and that this interaction may be hormonally modulated. To test this possibility a system has been developed in which an enriched schwannoma cell culture can be obtained and co-cultured with pure neurons.

scholarly journals Transposon Mutagenesis-Guided CRISPR/Cas9 Screening Strongly Implicates Dysregulation of Hippo/YAP Signaling in Malignant Peripheral Nerve Sheath Tumor Development

Cancers ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1584
Author(s):  
Germán L. Vélez-Reyes ◽  
Nicholas Koes ◽  
Ji Hae Ryu ◽  
Gabriel Kaufmann ◽  
Mariah Berner ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Schwann Cell ◽  
Peripheral Nerve ◽  
Cell Line ◽  
Schwann Cells ◽  
Tumor Suppressor Genes ◽  
Tumor Formation ◽  
Loss Of Function ◽  
Suppressor Genes ◽  
Nerve Sheath

Malignant peripheral nerve sheath tumors (MPNSTs) are highly aggressive, genomically complex, have soft tissue sarcomas, and are derived from the Schwann cell lineage. Patients with neurofibromatosis type 1 syndrome (NF1), an autosomal dominant tumor predisposition syndrome, are at a high risk for MPNSTs, which usually develop from pre-existing benign Schwann cell tumors called plexiform neurofibromas. NF1 is characterized by loss-of-function mutations in the NF1 gene, which encode neurofibromin, a Ras GTPase activating protein (GAP) and negative regulator of RasGTP-dependent signaling. In addition to bi-allelic loss of NF1, other known tumor suppressor genes include TP53, CDKN2A, SUZ12, and EED, all of which are often inactivated in the process of MPNST growth. A sleeping beauty (SB) transposon-based genetic screen for high-grade Schwann cell tumors in mice, and comparative genomics, implicated Wnt/β-catenin, PI3K-AKT-mTOR, and other pathways in MPNST development and progression. We endeavored to more systematically test genes and pathways implicated by our SB screen in mice, i.e., in a human immortalized Schwann cell-based model and a human MPNST cell line, using CRISPR/Cas9 technology. We individually induced loss-of-function mutations in 103 tumor suppressor genes (TSG) and oncogene candidates. We assessed anchorage-independent growth, transwell migration, and for a subset of genes, tumor formation in vivo. When tested in a loss-of-function fashion, about 60% of all TSG candidates resulted in the transformation of immortalized human Schwann cells, whereas 30% of oncogene candidates resulted in growth arrest in a MPNST cell line. Individual loss-of-function mutations in the TAOK1, GDI2, NF1, and APC genes resulted in transformation of immortalized human Schwann cells and tumor formation in a xenograft model. Moreover, the loss of all four of these genes resulted in activation of Hippo/Yes Activated Protein (YAP) signaling. By combining SB transposon mutagenesis and CRISPR/Cas9 screening, we established a useful pipeline for the validation of MPNST pathways and genes. Our results suggest that the functional genetic landscape of human MPNST is complex and implicate the Hippo/YAP pathway in the transformation of neurofibromas. It is thus imperative to functionally validate individual cancer genes and pathways using human cell-based models, to determinate their role in different stages of MPNST development, growth, and/or metastasis.

scholarly journals Interleukin-4 Regulates the Expression of CD209 and Subsequent Uptake of Mycobacterium leprae by Schwann Cells in Human Leprosy

2010 ◽  
Vol 78 (11) ◽  
pp. 4634-4643 ◽  
Author(s):  
Rosane M. B. Teles ◽  
Stephan R. Krutzik ◽  
Maria T. Ochoa ◽  
Rosane B. Oliveira ◽  
Euzenir N. Sarno ◽  
...  
Keyword(s):  
Schwann Cell ◽  
Peripheral Nerve ◽  
Schwann Cells ◽  
Primary Cultures ◽  
Mycobacterium Leprae ◽  
Microbial Pathogens ◽  
Interleukin 4 ◽  
Common Mechanism ◽  
Specific Cell

ABSTRACT The ability of microbial pathogens to target specific cell types is a key aspect of the pathogenesis of infectious disease. Mycobacterium leprae, by infecting Schwann cells, contributes to nerve injury in patients with leprosy. Here, we investigated mechanisms of host-pathogen interaction in the peripheral nerve lesions of leprosy. We found that the expression of the C-type lectin, CD209, known to be expressed on tissue macrophages and to mediate the uptake of M. leprae, was present on Schwann cells, colocalizing with the Schwann cell marker, CNPase (2′,3′-cyclic nucleotide 3′-phosphodiesterase), along with the M. leprae antigen PGL-1 in the peripheral nerve biopsy specimens. In vitro, human CD209-positive Schwann cells, both from primary cultures and a long-term line, have a higher binding of M. leprae compared to CD209-negative Schwann cells. Interleukin-4, known to be expressed in skin lesions from multibacillary patients, increased CD209 expression on human Schwann cells and subsequent Schwann cell binding to M. leprae, whereas Th1 cytokines did not induce CD209 expression on these cells. Therefore, the regulated expression of CD209 represents a common mechanism by which Schwann cells and macrophages bind and take up M. leprae, contributing to the pathogenesis of leprosy.

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