scholarly journals FINE STRUCTURAL ALTERATIONS ASSOCIATED WITH VENOM ACTION ON SQUID GIANT NERVE FIBERS

1968 ◽  
Vol 36 (2) ◽  
pp. 341-353 ◽  
Author(s):  
Rainer Martin ◽  
Philip Rosenberg

(1) Block of conduction and marked increase in permeability of the squid giant axon, when surrounded by adhering small nerve fibers, is caused by the venoms of cottonmouth, ringhals, and cobra snakes and by phospholipase A (PhA). This phenomenon is associated with a marked breakdown of the substructure of the Schwann sheath into masses of cytoplasmic globules. Low concentrations of these agents which render the axons sensitive to curare cause less marked changes in the structure of the sheath. (2) Rattlesnake venom, the direct lytic factor obtained from ringhals venom, and hyaluronidase caused few observable changes in structure, correlating with the inability of these agents to increase permeability. (3) Cottonmouth venom did not alter the structure of giant axons freed of all adhering small nerve fibers. This is in agreement with previous evidence that the venom effects are due to an action of lysophosphatides liberated as a result of PhA action. Cetyltrimethylammonium chloride, a cationic detergent, produces effects that resemble those of venom and PhA. (4) The results provide evidence that PhA is the component of the venoms that is responsible for their effects. It also appears that the Schwann cell and possibly the axonal membrane are the major permeability barriers in the squid giant axon.

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.


1963 ◽  
Vol 46 (5) ◽  
pp. 1065-1073 ◽  
Author(s):  
Philip Rosenberg ◽  
F. C. G. Hoskin

D-Tubocurarine (curare) and acetylcholine (ACh) had been found to block electrical activity after treatment of squid giant axons with cottonmouth moccasin venom at a concentration which had no effect on conduction. It has now been demonstrated that this effect is attributable to reduction of permeability barriers. The penetration of externally applied C14-labeled dimethylcurare, ACh, choline, and trimethylamine into the axoplasm of the squid giant axon was determined in axons treated with either cottonmouth, rattlesnake, or bee venom, and in untreated control axons. The lipid-soluble tertiary nitrogen compound trimethylamine readily penetrated into the axoplasm of untreated axons. In contrast, after exposure of the axons to the lipid-insoluble quaternary nitrogen compounds for 1 hour their presence in the axoplasm was hardly detectable (less than 1 per cent). However, following 15µg/ml cottonmouth venom 1 to 5 per cent of their external concentration is found within the axoplasm while following 50µg/ml venom 10 to 50 per cent enters. The penetration of dimethylcurare is also increased by 10 µg/ml bee venom but not by 1 µg/ml bee venom nor 1000 µg/ml rattlesnake venom. The experiments show that when ACh and curare, following venom treatment, affect electrical activity, they also penetrate into the axon. Treatments which do not increase penetration are also ineffective in rendering the compounds active.


Author(s):  
J. Metuzals

It has been demonstrated that the neurofibrillary tangles in biopsies of Alzheimer patients, composed of typical paired helical filaments (PHF), consist also of typical neurofilaments (NF) and 15nm wide filaments. Close structural relationships, and even continuity between NF and PHF, have been observed. In this paper, such relationships are investigated from the standpoint that the PHF are formed through posttranslational modifications of NF. To investigate the validity of the posttranslational modification hypothesis of PHF formation, we have identified in thin sections from frontal lobe biopsies of Alzheimer patients all existing conformations of NF and PHF and ordered these conformations in a hypothetical sequence. However, only experiments with animal model preparations will prove or disprove the validity of the interpretations of static structural observations made on patients. For this purpose, the results of in vitro experiments with the squid giant axon preparations are compared with those obtained from human patients. This approach is essential in discovering etiological factors of Alzheimer's disease and its early diagnosis.


1990 ◽  
Vol 1023 (3) ◽  
pp. 421-435 ◽  
Author(s):  
Harvey M. Fishman ◽  
Kirti P. Tewari ◽  
Philip G. Stein
Keyword(s):  

2004 ◽  
Vol 207 (2) ◽  
pp. 164-164
Author(s):  
Michael P. Conley ◽  
Marcus K. Jang ◽  
Joseph A. DeGiorgis ◽  
Elaine L. Bearer

1978 ◽  
Vol 54 (6) ◽  
pp. 310-315 ◽  
Author(s):  
Tohru YOSHIOKA ◽  
Toshifumi TAKENAKA ◽  
Hidenori HORIE ◽  
Hiroko INOUE ◽  
Kimie INOMATA

2002 ◽  
Vol 203 (2) ◽  
pp. 189-190 ◽  
Author(s):  
Antonio Giuditta ◽  
Maria Eyman ◽  
Barry B. Kaplan

Neuroscience ◽  
1999 ◽  
Vol 90 (2) ◽  
pp. 705-715 ◽  
Author(s):  
J.R Sotelo ◽  
A Kun ◽  
J.C Benech ◽  
A Giuditta ◽  
J Morillas ◽  
...  

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