scholarly journals Autoradiographic localization of acetylcholine receptors in the Schwann cell membrane of the squid nerve fiber

1978 ◽  
Vol 77 (2) ◽  
pp. 371-376 ◽  
Author(s):  
FA Rawlins ◽  
J Villegas

Intact and slit nerve fibers of the squid Sepioteuthis sepioidea were incubated in a 50-nM solution of [125I] alpha-bungarotoxin in artificial seawater, in the absence and in the presence of D-tubocurarine (10(-4) M). The distribution of the radioactive label was then determined by electron microscope autoradiography. It was found that, in the fibers exposed solely to the radioactive toxin, the label was located mainly at the axon-Schwann cell boundary in the intact nerve fibers or at the axonal edge of the Schwann cell layer in the axon-free nerve fiber sheaths. Label was also present in those regions of the Schwann cell layer rich in intercellular channels. No signs of radioactivity were observed in the nerve fibers exposed to the labeled toxin in the presence of D-tubocurarine. These results indicate that the acetycholine receptors previously found in the Schwann cell plasma membrane are mainly located over the cell surfaces facing the neighboring axon and the adjacent Schwann cells. These findings represent a further advance in the understanding of the relationship between the axon and its satellite Schwann cell.

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.


1973 ◽  
Vol 58 (1) ◽  
pp. 42-53 ◽  
Author(s):  
Frank A. Rawlins

A time-sequence study of the incorporation and distribution of cholesterol in peripheral nerve myelin was carried out by electron microscope autoradiography. [1,2-3H]Cholesterol was injected into 10-day old mice and the sciatic nerves were dissected out at 10, 20, 40, 60, 90, 120, and 180 min after the injection. 20 min after injection the higher densities of grains due to the presence of [3H]cholesterol were confined to the outer and inner edges of the myelin sheath. Practically no cholesterol was detected in the midzone of the myelin sheath. 1 ½ h after injection, cholesterol showed a wider distribution within the myelin sheath, the higher densities of grains occurring over the two peripheral myelin bands, each approximately 3,100 Å wide. Cholesterol was also present in the center of the myelin sheath but to a considerably lesser extent. 3 h after injection cholesterol appeared homogeneously distributed within the myelin sheath. Schwann cell and axon compartments were also labeled at each time interval studied beginning 20 min postinjection. These observations indicate that preformed cholesterol enters myelin first and almost simultaneously through the inner and outer edges of the sheath; only after 90 min does the density of labeled cholesterol in the central zone of myelin reach the same density as that in the outer and inner zones. These findings suggest that cholesterol used by the nerve fibers in the formation and maintenance of the myelin sheath enters the lamellae from the Schwann cell cytoplasm and from the axon. The possibility of a bidirectional movement of molecules, i.e. from the Schwann cell to the axon and from the axon to the Schwann cell through the myelin sheath, is noted. The results are discussed in the light of recent observations on the exchange, reutilization, and transaxonal movement of cholesterol.


PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0158083 ◽  
Author(s):  
Ekaterina E. Verdiyan ◽  
Elvin S. Allakhverdiev ◽  
Georgy V. Maksimov

1983 ◽  
Vol 96 (6) ◽  
pp. 1781-1785 ◽  
Author(s):  
M M Salpeter ◽  
R Harris

The distribution and turnover rate of acetylcholine receptors labeled with 125I-alpha-bungarotoxin were examined in innervated mouse sternomastoid muscle by electron microscope autoradiography using the "mask" analysis procedure. We compared the total population of receptors with receptors newly inserted at the junction 2 d after inactivation with nonradioactive alpha-bungarotoxin, both at the top (thickened) region of the postjunctional folds (pjm) and the nonthickened bottom folds. We found that the receptor site density was approximately 10 times greater on the thickened pjm than on the nonthickened bottom folds for both total and newly inserted receptors. This ratio does not change significantly during a 6-d period after labeling the new receptors. Furthermore, calculated values for turnover time of receptors show that both total and newly inserted receptors at both regions of the junctional folds have half-lives for degradation within the range given in the literature for slow junctional receptors. These data exclude a simple migration model whereby receptors are preferentially inserted in the nonthickened region of the junctional folds and then migrate into the thickened membrane at a rate equal to the turnover rate of the receptors.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Abdelrahman M. Alhilou ◽  
Akiko Shimada ◽  
Camilla I. Svensson ◽  
Peter Svensson ◽  
Malin Ernberg ◽  
...  

AbstractThe neurophysiological mechanisms underlying NGF-induced masseter muscle sensitization and sex-related differences in its effect are not well understood in humans. Therefore, this longitudinal cohort study aimed to investigate the effect of NGF injection on the density and expression of substance P, NMDA-receptors and NGF by the nerve fibers in the human masseter muscle, to correlate expression with pain characteristics, and to determine any possible sex-related differences in these effects of NGF. The magnitude of NGF-induced mechanical sensitization and pain during oral function was significantly greater in women than in men (P < 0.050). Significant positive correlations were found between nerve fiber expression of NMDA-receptors and peak pain intensity (rs = 0.620, P = 0.048), and expression of NMDA-receptors by putative nociceptors and change in temporal summation pain after glutamate injection (rs = 0.561, P = 0.003). In women, there was a significant inverse relationship between the degree of NGF-induced mechanical sensitization and the change in nerve fiber expression of NMDA-receptors alone (rs = − 0.659, P = 0.013), and in combination with NGF (rs = − 0.764, P = 0.001). In conclusion, women displayed a greater magnitude of NGF-induced mechanical sensitization that also was associated with nerve fibers expression of NMDA-receptors, when compared to men. The present findings suggest that, in women, increased peripheral NMDA-receptor expression could be associated with masseter muscle pain sensitivity.


1996 ◽  
Vol 13 (5) ◽  
pp. 991-994 ◽  
Author(s):  
B. Ehinger ◽  
C. L. Zucker

AbstractTwo synapse-rich layers are well recognized in the mammalian retina, the inner and outer plexiform layers. However, synapses occur also in other layers, particularly in the innermost nerve fiber layer. These synapses form a tenuous layer at times referred to as the superficial plexiform layer. We have found that staining for GABAA receptors in whole-mounted rabbit retina demonstrates this layer. It is most well developed in the region of the visual streak 2–4 mm below the center of the myelinated streak and is very sparse in other parts. Most or all of the processes in the plexus originate from cells in the ganglion cell layer.


2018 ◽  
Vol 3 ◽  
pp. 20 ◽  
Author(s):  
Diane L. Sherman ◽  
Peter J. Brophy

Charcot-Marie-Tooth (CMT) disease comprises up to 80 monogenic inherited neuropathies of the peripheral nervous system (PNS) that collectively result in demyelination and axon degeneration. The majority of CMT disease is primarily either dysmyelinating or demyelinating in which mutations affect the ability of Schwann cells to either assemble or stabilize peripheral nerve myelin. CMT4F is a recessive demyelinating form of the disease caused by mutations in the Periaxin (PRX) gene. Periaxin (Prx) interacts with Dystrophin Related Protein 2 (Drp2) in an adhesion complex with the laminin receptor Dystroglycan (Dag). In mice the Prx/Drp2/Dag complex assembles adhesive domains at the interface between the abaxonal surface of the myelin sheath and the cytoplasmic surface of the Schwann cell plasma membrane. Assembly of these appositions causes the formation of cytoplasmic channels called Cajal bands beneath the surface of the Schwann cell plasma membrane. Loss of either Periaxin or Drp2 disrupts the appositions and causes CMT in both mouse and man. In a mouse model of CMT4F, complete loss of Periaxin first prevents normal Schwann cell elongation resulting in abnormally short internodal distances which can reduce nerve conduction velocity, and subsequently precipitates demyelination. Distinct functional domains responsible for Periaxin homodimerization and interaction with Drp2 to form the Prx/Drp2/Dag complex have been identified at the N-terminus of Periaxin. However, CMT4F can also be caused by a mutation that results in the truncation of Periaxin at the extreme C-terminus with the loss of 391 amino acids. By modelling this in mice, we show that loss of the C-terminus of Periaxin results in a surprising reduction in Drp2. This would be predicted to cause the observed instability of both appositions and myelin, and contribute significantly to the clinical phenotype in CMT4F.


1992 ◽  
Vol 20 (01) ◽  
pp. 25-35 ◽  
Author(s):  
Michio Kimura ◽  
Kazuo Tohya ◽  
Kyo-ichi Kuroiwa ◽  
Hirohisa Oda ◽  
E. Christo Gorawski ◽  
...  

During a sparrow-pecking and twisting-needle manipulation to the acupoints BL 23, 24 and 25 for an induction of "Qi", it was found that some transparent materials were binding to the needles after removed from the volunteer's skin. Electron-microscopical analysis of the transparent materials revealed that they corresponded to the injured fascia made up of collagen fibers, elastic fibers, fibroblasts, adipocytes and mast cells. Rarely were nerve fiber-like structures observed in the materials. Immunohistochemically, calcitonin gene-related peptide-positive nerve fibers could be demonstrated in the acupoint BL 24 associated fascia. A possible functional relationship between the needle manipulation and the induction of Qi-sensation is discussed along with the acupoint tissue constitution.


1988 ◽  
Vol 1 (2) ◽  
pp. 245-248 ◽  
Author(s):  
Glen T. Prusky ◽  
Max S. Cynader

AbstractThe autoradiographic distribution of [3H]nicotine binding sites was examined in the superior colliculus in normal rats and cats, and in animals in which one or both eyes were removed. [3H]Nicotine binding sites in normal animals were densely concentrated in the superficial layers of the colliculus corresponding to the zone of termination of optic nerve fibers. Following bilateral enucleation, [3H]nicotine binding in the superficial collicular layers was drastically reduced. Unilateral enucleation markedly reduced [3H]nicotine binding sites in the colliculus contralateral to the removed eye, with little effect on the ipsilateral colliculus. These results provide further evidence that nicotinic acetylcholine receptors have a presynaptic location on optic tract terminals and may therefore modulate retinotectal transmission in both the rat and cat visual system.


Sign in / Sign up

Export Citation Format

Share Document