Electrical conduction through nerve and DNA

The aim of the present study was to analyse electric resistivity at different ambient temperatures between 300 to 20K in the frog sciatic nerve and salmon sperm DNA. When the electrical contacts were leaned just into the sciatic nerve, an increase of the sciatic nerve resistivity was observed for 240 K < T < 300 K and a rise of electrical conductivity was apparent below 240 K. This dependence is generally associated with a semiconductor behaviour. Once the sciatic nerve temperature was driven below 250K, the resistivity abruptly decreased and then at temperatures lower than 234 K, it remained constant and close to one tenth of its ambient temperature value. By contrast, when the electrical contacts were leaned into Salmon sperm DNA, the resistivity remained constant between 300K to 20K, showing a high electrical stability at low temperature. Thus, we report the existence of a new form of electric conductivity in the sciatic nerve at low ambient temperature, which in turn has many electric similarities with inorganic or organic superconductors, whereas temperature failed to alter DNA electrical properties until 20K.     

神经传导的新概念:无动作电位的兴奋传导

近年来研究揭示在神经传导中存在着无动作电位的兴奋传导机制,它主要涉及细胞膜中胞膜窖专门化脂筏内的分子转导作用,这对兴奋只能通过电现象沿神经进行传导的传统理念是一个重大的挑战.这一机制可能是神经科学基础领域研究的重要进展.     

Stretch-induced nerve conduction deficits in guinea pig ex vivo nerve

In the current communication, we characterized supraphysiologic elongations that elicited short-term nerve dysfunction. This was accomplished by assessing the electrophysiology of guinea pig tibial and peroneal nerves at predetermined elongation magnitudes. Results showed that a longitudinal supraphysiological stretch of lambda = 1.05 caused a 16% reduction in the mean compound action potential (CAP) amplitude. Upon relaxation to physiologic length, a full recovery in the CAP was observed. At lambda = 1.10, the CAP decreased by 50% with an 88% recovery after relaxation. For a supraphysiologic stretch of lambda = 1.20, severe conduction block with minimal acute recovery was observed. Latency also increased during periods of stretch and was proportional to the stretch magnitude. Additional studies showed some electrophysiological recovery during the sustained stretch phase. This attribute may be related to internal stress relaxation mechanisms. Since whole nerve elongations are averaged global deformations, we also used an incremental digital image correlation (DIC) technique to characterize the strain at the micro-tissue level. The DIC analysis revealed considerable heterogeneity in the planar strain field, with some regions exhibiting strains above the macroscale stretch. This non-uniformity in the strain map arises from structural inconsistencies of the nerve and we presume that zones of high local strain may translate into the observed conduction deficits.     

On the formal theory of nerve conduction

A general solution of the formal nerve conduction problem is given. As illustrations of the general method, the capacitative single-factor and the non-capacitative Lapicque problems are solved. Comparisons between velocity formulae for capacitative and non-capacitative models indicate that previously determined non-capacitative velocities are considerably too high.     

On the cable theory of nerve conduction

Conduction of an impulse in the nonmyelinated nerve fiber is treated quantitatively by considering it as a direct consequence of the coexistence of two structurally distinct regions, resting and active, in the fiber. The profile of the electrical potential change induced in the vicinity of the boundary between the two regions is analyzed by using the cable equations. Simple mathematical formulae relating the conduction velocity to the electrical parameters of the fiber are derived from the symmetry of the potential profile at the boundary. The factors that determine the conduction velocity in the myelinated nerve fiber are reexamined.     

Molecular mechanisms of nerve excitation and conduction

In this paper we propose that the physical behavior of the electric dipoles at the membraneinterface is mainly responsible for the observed phenomena in nerve excitation and conduction. The underlying molecular mechanisms are conceived to be dipole reorientation, relaxation and flip-flops. It is suggested that quantum transitions of electric dipoles and a few first principles provide a real physical basis for the neural behavior as manifested macroscopically. This dipole theory gains a strong support from the most recent discoveries of negative fixed surface charge on axon membranes, infrared emission from stimulated nerve and the birefringence change which coincided with the action potential in squid axon. It can also offer an explanation for the heat production and absorption in excited nerves. A brief discussion will be given to the memory mechanism in terms of the field-dipole interaction during the RNA synthesis in nerve cells. Visiting the Research Institute of Electronics, Chiao-Tung University, Hsinchu, Formosa (Taiwan), September 1, 1968–June 1, 1969.     

Sorbitol, inositol and nerve conduction in diabetes

Motor nerve conduction velocity was lower in streptozotocin-diabetic rats than in controls. Treatment with the aldose reductase inhibitor Sorbinil restored conduction velocity to normal. Diabetic rats had an increased concentration of sorbitol and reduced free inositol in sciatic nerve. Sorbinil corrected both defects. Inositol administration to diabetic rats also restored conduction velocity to normal. Genetically diabetic mice had reduced concentrations of inositol in sciatic nerve but fructose and sorbitol were normal. Glucose concentration was considerably increased.     

Constant magnetic field and nerve impulse conduction]

It is shown that external magnetic field produces no ponderomotor effect on the nerve fibre along which the impulse propagates.     

Continuous conduction of impulses in peripheral myelinated nerve fibers

1. Conduction of impulses in peripheral myelinated fibers of a nerve trunk is a continuous process, since with uninjured nerve fibers: (a) within each internodal segment the conduction time increases continuously and linearly with increasing conduction distance; (b) the presence of nodes of Ranvier does not result in any detectable discontinuity in the conduction of the impulse; (c) the ascending phase of the spike always has an S shape and never presents signs of fractionation; (d) the shape and magnitude of the spike are constant at all points of each internodal segment. 2. Records have been presented of the external logitudinal current that flows during propagation of an impulse in undissected single nerve fiber (Fig. 6). 3. Propagation of impulses across a conduction block occurs with a readily demonstrable discontinuity.     

Apparent rapid tolerance to ethanol for nerve conduction velocity

Apparent rapid tolerance to ethanol for decrease in nerve conduction velocity, lasting up to one day but to seven days, was shown in HS mice following a single injection (i.p.) of 3.0 g EtOH/kg body wt. Relative conduction time (RCT-reciprocal of velocity) was studied in the caudal nerves of 60 mice. In Exp. 1 30 mice were tested twice, 7 days apart; these showed no significant change in RCT on re-test. In Exp. 2 30 mice tested twice, 1 day apart, showed a significantly smaller response to ethanol in the second test. This result suggests that ethanol tolerance in peripheral nerve conduction velocity may develop in these mice after a single ethanol dose. In addition, ethanol effects on two measures of CNS depression also suggest tolerance after one day and lasting to seven days. The basis for these apparent examples of tolerance to ethanol is not clear.     

Analysis of nerve conduction block induced by direct current

The mechanisms of nerve conduction block induced by direct current (DC) were investigated using a lumped circuit model of the myelinated axon based on Frankenhaeuser–Huxley (FH) model. Four types of nerve conduction block were observed including anodal DC block, cathodal DC block, virtual anodal DC block, and virtual cathodal DC block. The concept of activating function was used to explain the blocking locations and relation between these different types of nerve block. Anodal/cathodal DC blocks occurred at the axonal nodes under the block electrode, while virtual anodal/cathodal DC blocks occurred at the nodes several millimeters away from the block electrode. Anodal or virtual anodal DC block was caused by hyperpolarization of the axon membrane resulting in the failure of activating sodium channels by the arriving action potential. Cathodal or virtual cathodal DC block was caused by depolarization of the axon membrane resulting in inactivation of the sodium channel. The threshold of cathodal DC block was lower than anodal DC block in most conditions. The threshold of virtual anodal/cathodal blocks was about three to five times higher than the threshold of anodal/cathodal blocks. The blocking threshold was decreased with an increase of axonal diameter, a decrease of electrode distance to axon, or an increase of temperature. This simulation study, which revealed four possible mechanisms of nerve conduction block in myelinated axons induced by DC current, can guide future animal experiments as well as optimize the design of electrodes to block nerve conduction in neuroprosthetic applications.     

Motor and sensory nerve conduction velocities in Yucatan minipigs

Motor and/or sensory conduction velocities are used to assess peripheral nervous system disorders. Although the miniature pig represents a model of choice for long-term pharmacological experimentation, no study has so far been reported on this model in relation to the measurement of nerve conduction velocities. We developed the present technique and applied it to 34 3-18-month-old Yucatan minipigs. Motor and sensory conduction velocities were measured using the anterior tibial nerve and the internal plantar nerve, a branch of the posterior tibial nerve, respectively. The nerve conduction velocity data of motor (MNCV) and sensory (SNCV) nerves, together with the amplitude of the sensory nerve signal, were logarithmically dependent on the age of the tested animals (r(2)=0.92, 0.81 and 0.76, respectively). The mean values of MNCV and SNCV were 70.9 +/- 1.1 and 67.9 +/- 0.2 m/s, respectively, at the age of 16 months for these miniature pigs. In order to validate this model, we compared it with other known models when the velocities reached a plateau at the end of the study. These values were found to be higher than those in humans or rats, but are comparable to those of the baboon, one of the best large animal models for human pathologies. Because the physiology and metabolism of the minipig resemble those of humans, and due to its long lifetime, this animal represents a good model for studying the development of neuropathology.     

Contribution of circulating acetylcholine to sensory nerve conduction augmentation

We previously discovered that sensory nerve action potential amplitudes increased during isometric muscle contraction and that this response could be blocked with tourniquet isolation of the contraction source. The hypothesis for this study was that a circulating factor was responsible for this effect. In this prospective study, baseline and post intravenous injection of serial sural nerve action potential recordings were made in the leg of 8 rabbits. The sequence of the injections was randomized: 1) normal saline placebo, 2) 0.01 mg/kg acetylcholine (ACh) 3) 200 mg/kg Na acetate, 4) 260 mg/kg Na lactate, and 5) 20 mg/kg choline. Results showed there was a 3.8 microV increase in the sural nerve response 6 min after ACh injection compared to baseline at rest (p = .01, power = .9, analysis of variance (ANOVA), repeated measures). There were no significant changes in the amplitudes of the sural nerve after injection of the remaining agents or placebo (p = .33 to .81, ANOVA, repeated measures). In conclusion, circulating ACh is the only agent tested thus far that appears to be responsible for this effect. In addition, the amplitude and temporal curve of this response is similar to that seen after exercise in human subjects. The clinical importance of this study is that ACh plays a role in this newly discovered sensory regulatory mechanism controlled by the motor system.     

Comparison of magnetic and electrical phrenic nerve stimulation in assessment of phrenic nerve conduction time

Similowski, Thomas, Selma Mehiri, Alexandre Duguet,Valérie Attali, Christian Straus, and Jean-Philippe Derenne.Comparison of magnetic and electrical phrenic nerve stimulation inassessment of phrenic nerve conduction time. J. Appl.Physiol. 82(4): 1190-1199, 1997.Cervicalmagnetic stimulation (CMS), a nonvolitional test of diaphragm function,is an easy means for measuring the latency of the diaphragm motorresponse to phrenic nerve stimulation, namely, phrenic nerve conductiontime (PNCT). In this application, CMS has some practical advantagesover electrical stimulation of the phrenic nerve in the neck (ES).Although normal ES-PNCTs have been consistently reported between7 and 8 ms, data are less homogeneous for CMS-PNCTs, with some reportssuggesting lower values. This study systematically compares ES-and CMS-PNCTs for the same subjects. Surface recordings ofdiaphragmatic electromyographic activity were obtained for sevenhealthy volunteers during ES and CMS of varying intensities. Onaverage, ES-PNCTs amounted to 6.41 ± 0.84 ms and were littleinfluenced by stimulation intensity. With CMS, PNCTs were significantlylower (average difference 1.05 ms), showing a marked increase as CMSintensity lessened. ES and CMS values became comparable for a CMSintensity 65% of the maximal possible intensity of 2.5 Tesla. Thesefindings may be the result of phrenic nerve depolarization occurringmore distally than expected with CMS, which may have clinicalimplications regarding the diagnosis and follow-up of phrenic nervelesions.

     

A study of conduction velocity in nonmyelinated nerve fibers.

By treating a nonmyelinated nerve fiber as a continuous cable consisting of three distinct zones (Resting, transitional, and excited), the following mathematical expression was derived: (formula: see text) where v is the conduction velocity, d the diameter of the fiber, R the resistance of the membrane of unit area at the peak of excitation, rho the resistivity of the medium inside the fiber, and C the capacity of membrane per unit area. The validity of this expression was demonstrated by using squid giant nerve fibers intracellularly perfused with dilute salt solutions. The relationship between these results and previous theories and experiments on conduction velocity is discussed.