In Vitro Experiments of Information Transmission in a Frog Sciatic Nerve

Author(s):  
M. Hannula ◽  
E. Alasaarela ◽  
J. Tikkanen ◽  
A. Makynen ◽  
R. Myllyla
1983 ◽  
Vol 244 (1) ◽  
pp. C75-C81 ◽  
Author(s):  
P. Ask ◽  
H. Levitan ◽  
P. J. Robinson ◽  
S. I. Rapoport

Measurements of volume and hydrostatic pressure in the frog sciatic nerve in vitro demonstrate that the nerve acts as an osmometer, in large part because the perineurium is a semipermeable membrane for water flow. Endoneurial hydrostatic pressure in nerves in isotonic Ringer exceeds bath pressure by about 7 mmHg. In Ringer made hypertonic by addition of sucrose, nerve volume and endoneurial pressure fall linearly in relation to 1/osmolality. The slope of the plot of pressure against volume provides a value for nerve compliance equal to 0.006 mm2/mmHg. Calculations based on the model of the nerve as an osmometer indicate that the nerve has an osmotically "inactive" volume equal to 0.19 mm3/mm, which is about 75% of the total volume of a nerve segment of unit length in normal Ringer. Perineurial hydraulic conductivity (Lp) equals 7.5 x 10(-13) cm3.s-1.dyn-1, a value characteristic of nonleaky epithelia. The perineurium is an elastic tissue with a constant modulus of elasticity equal to 3 x 10(6) dyn/cm2 when not markedly stretched and may limit nerve swelling under pathological conditions of nerve edema.


1972 ◽  
Vol 60 (4) ◽  
pp. 388-405 ◽  
Author(s):  
Lester M. Partlow ◽  
C. David Ross ◽  
Ratna Motwani ◽  
David B. McDougal

Redistribution of axonal enzymes as a function of time in vitro was studied in an unbranched segment of frog sciatic nerve. Cholinesterase activity moved peripherally at a rate of 99 mm/day and centrally at 19 mm/day. One-quarter of the total nerve content of the enzyme was estimated to be in motion, one-eighth in each direction. Mitochondrial enzymes (hexokinase and glutamic dehydrogenase) moved peripherally at 20–31 mm/day, centrally at 11–20 mm/day. Only 10% of the total content of these mitochondrial enzymes was in motion. No movement of choline acetylase or 6-phosphogluconic dehydrogenase activity was seen even after 4 days in vitro. However, in a 12 day in vivo experiment choline acetylase moved toward the periphery at a rate of 0.34 mm/day. After a day or so in vitro the distal accumulations of cholinesterase and glutamic dehydrogenase decreased, with a concomitant and quantitatively equivalent increase in enzyme activities at the proximal end of the nerve. It is postulated that during incubation a mechanism for reversing the direction of flow develops in the peripheral stump of the nerve. Vinblastine inhibited central and peripheral flow of both cholinesterase and glutamic dehydrogenase. Movement of cholinesterase was not affected by ouabain, thalidomide, or phenobarbital, nor by K+ excess (110 mM) or absence.


1988 ◽  
Vol 90 (1-2) ◽  
pp. 113-118 ◽  
Author(s):  
Anders Edström ◽  
Martin Kanje

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.


2008 ◽  
Author(s):  
Nichole M. Jindra ◽  
Robert J. Thomas ◽  
Douglas N. Goddard ◽  
Michelle L. Imholte

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