Conduction In Nerve Fibers Research Articles

Dependence of the linear model for the nerve compound action potential on the single fibre action potential waveform

The linear model of the nerve compound action potential (CAP) depends on the assumed waveform for the single fibre action potential (SFAP). A general method has been developed to investigate the influence of the unknown features of the SFAP on the estimation of nerve fibre conduction velocity (CV) distribution. A SFAP waveform is considered consistent with the model and the experimental data if recorded and reconstructed CAPS fit and the distribution is physically meaningful. Experimental CAPS were monopolarly recorded using surface electrodes over the median nerve at the wrist. To fit the model, SFAP waveforms must satisfy some internal relationship. The most important feature is that the ratio between positive and negative areas of the SFAP is almost one and does not vary in different subjects and recording sites. Many SFAP waveforms fit the model, and the relative conduction velocity distributions may be very different. These must be regarded as conventional distributions. As for inter-subject comparison, the dependence of the method on the recording site has been reduced by choosing the place where stimulus intensity and relative motor response amplitude have given values. In this recording environment CV distributions of normal subjects can be properly compared using the same SFAP and deviations from normality evidenced.

Effects of lead exposure on peripheral nerve in the cynomolgus monkey.

The relationship between blood lead concentration and nerve conduction velocity has been examined, using the cynomolgus monkey as a model for human lead poisoning, with lead dose and blood lead concentration maintained under controlled conditions, to determine whether nerve conduction velocity could be used as an objective measure of the effects of lead on the nervous system at subclinical concentrations. Five cynomolgus monkeys were maintained at a blood lead concentration of 90-100 micrograms Pb/100 ml for nine months by daily oral dosing with lead acetate (12-15 mg Pb/kg body weight). Motor nerve conduction velocity in the ulnar nerve was measured, together with blood lead concentrations. Blood lead concentrations were proportional to lead intake, reaching a stable level within one to two weeks. Lead did not accumulate in the blood, and blood lead concentrations were found to decrease to a maintained plateau from initial high concentrations during the first seven days of dosing. The animals showed no clinical or behavioural evidence of lead poisoning at any time during the study, although there was a progressive decrease in blood packed cell volume, haemoglobin concentration, and erythrocyte concentration. The maximal motor nerve conduction velocity of the ulnar nerve remained constant throughout the study, although changes were observed in the conduction velocity of slowly conducting nerve fibres. At termination, intranuclear inclusions were found in the renal tubular cells of all animals as were focal areas of myelin degeneration in the ulnar and sciatic nerves.

Nerve-fiber conduction velocity distributions in the median nerve bundle

Nerve-fiber conduction velocity distributions in the median nerve bundle

Studies of diabetic polyneuropathy using conduction velocity distribution (DCV) analysis.

The distributions of nerve fiber conduction velocities (DCVs) derived from the median nerves of 29 adult diabetic patients (mean age, 52.1 +/- 12.3 years) with mild or no symptoms or signs of polyneuropathy were compared with DCVs from 34 age-appropriate normal subjects. Ten patients (34%) had normal findings (type A DCVs). In the 19 patients (66%) with abnormal DCVs, defined as 10% or more of the DCV area falling outside the normal 95% confidence limits, two distinct patterns of DCV alteration were observed: type B DCVs (11 patients) showed reduced DCVmax, DCVmean, and DCVpeak, together with reduced DCVrange (narrow profile); whereas type C DCVs (8 patients) had reduced DCVmax, DCVmean, DCVpeak, and DCVmin, with normal DCVrange (broad profile). It is proposed that type C DCV represents a more advanced form of type B and that both reflect selective dysfunction of the fastest conducting (presumably largest-diameter) fibers in the nerve trunk. DCVmax was consistently greater than conventional measures of "maximal" CV in all patient subgroups. Patients with abnormal DCVs had higher incidence of mild neuropathic symptoms (15 of 19 versus 4 of 10, p less than 0.01) and greater insulin dependence (11 of 19 versus 1 of 10, p less than 0.001). Serial studies in 10 patients showed, at most, small degrees of change in conduction properties over relatively short intervals (1 to 9 months).

The effect of capsaicin application to a peripheral nerve on impulse conduction in functionally identified afferent nerve fibres

Capsaicin applied locally to a coccygeal or saphenous nerve of rats was shown to block impulse conduction in unmyelinated afferent nerve fibres. Shortly after application of capsaicin (1% dissolved in 10% Tween 80 in paraffin oil) conduction of C-fibre— but not A-fibre — compound action potentials across the application site was markedly diminished. No recovery occurred during the period of observation, i.e. up to 2 h afterwards. C-Fibre compound action potentials stimulated and recorded proximal to the application site seemed to be unaffected. Solvent application had no effect. Recording from single units revealed that nociceptive C-fibres responding to strong mechanical and heat stimulation (MH units, polymodal nociceptors) were blocked. In contrast, unmyelinated cold fibres were not affected. The selective block of MH units indicates different membrane properties of unmyelinated MH and cold units not only at the receptive nerve endings, but also at the axons, to which capsaicin was applied.

The relationship between axon diameter, myelin thickness and conduction velocity during atrophy of mammalian peripheral nerves

The atrophy of cutaneous (sural) and muscle (medial gastrocnemius) nerves proximal to a ligation were studied in cats for periods up to 9 months, using light and electron microscopy, conduction velocity measurements and computer simulations. As atrophy proceeds, nerve fibres become increasingly non-circular. Cross-sectional areas of axons and fibres (axon + myelin) were measured. The diameters of equivalent circles (having the same axon and fibre cross-sectional area) were then calculated. A linear relation was found between axon diameter and fibre diameter, but the slope decreased as atrophy continued. This indicates that the axon cross-sectional area decreases relatively more than the total fibre area. Reduction in conduction velocity correlates more closely with reduction in axon diameter than fibre (axon + myelin) diameter. The ratio of the inner (axon) perimeter to the outer (myelin) perimeter remains constant at or near the optimal value of 0.6 for conduction in all groups of fibres at all periods of atrophy. Futhermore, the thickness of the myelin remains constant for a given perimeter over the entire period of atrophy studied. This suggests that the number of turns of myelin and the length of each turn remain unchanged during peripheral nerve atrophy. A simple geometric model explains how this can occur without gaps developing between the axon and myelin or between the turns of myelin. The Frankenhaeuser-Huxley equations for conduction in myelinated nerve fibres predict changes in conduction velocity similar to those observed, if the axons atrophy without changes in myelin. The advantages of this mode of atrophy are discussed.

Sites of actions of adenosine in intrinsic cholinergic nerves of ileal longitudinal muscle from guinea pig.

The sites of presynaptic actions of adenosine on electrically stimulated longitudinal muscle strip of guinea pig ileum were studied with a special dual organ bath. Local stimulation (0.1 Hz) of the anal part of the strip induced a twitch response in the stimulated part and in the non-stimulated oral part; both of these twitch responses were depressed by an application of adenosine to the anal, stimulated part of the strip. The present results suggested that electrical stimulation applied to the anal part of the strip travelled along the network of Auerbach's plexus in the oral direction, and adenosine might depress such conduction in cholinergic nerve fibers in addition to nerve terminals.

Conduction block in rat myelinated fibres following acute exposure to antigalactocerebroside serum

1. We have observed conduction in single rat spinal ventral root nerve fibres following acute topical application of anti-galactocerebroside serum.2. Conduction of nerve impulses was initially slowed and subsequently blocked at the site of serum exposure.3. Conduction block occurred within as little as 1 hr in more slowly conducting (20-30 m/sec) myelinated fibres but occurred later in fibres conducting more rapidly.4. Conduction block was preceded by a rise in internodal conduction time from the normal 20 musec to about 200 musec.5. At nodes exposed to serum, conduction block was invariably associated with greatly decreased depolarization; this was contrasted with nodes exposed to local anaesthetic or tetrodotoxin where conduction block occurred despite nodal depolarization well beyond threshold potential.6. Nodal capacitance and resistance were estimated from simultaneous recordings of membrane current and extracellular potential at blocked nodes exposed to local anaesthetic or tetrodotoxin (normal nodes) and at blocked nodes exposed to anti-galactocerebroside serum.7. For normal fibres of internodal length 0.8-1.1 mm, an upper limit estimate for average nodal capacitance was 2.6 +/- 0.3 pF and a lower limit estimate for average nodal resistance was 55 +/- 10 MOmega. There was an order of magnitude increase in the capacitance of nodes at which conduction block occurred following exposure to anti-galactocerebroside serum.8. We conclude that the early conduction block caused by anti-galactocerebroside serum is due to paranodal demyelination and that acute paranodal demyelination is sufficient to cause conduction block.

Acute effects of ethanol in vivo on neuromuscular transmission

The effects in vivo of acute doses of ethanol on impulse transmission in the region of the neuromuscular junction are poorly known. These effects were studied with a new procedure, using mouse tails in a constant temperature chamber to study the delay in nerve-to-muscle impulse transmission. A saline control and five ethanol doses (0.5, 1.0, 1.4, 2.0, 4.24 g/kg) were used with 96 mice. The interval ("residual latency", RL), between (a) the peak of the compound nerve action potential and (b) the first peak of the associated compound muscle action potential, was measured. Ethanol was given IP and tail nerve stimulations were done at 4 min intervals to 16 min post-ethanol. The mean pre-ethanol RL was 0.93 +/- 0.01 (SE) msec; about 25% of this time should be synaptic delay and the remainder is nerve and muscle fiber conduction time. Individual post-ethanol relative RL (RRL) values were calculated for each moue, based on its pre-ethanol value. With doses of 1.0 g/kg and higher there was a mean increase in RRL; at 16 min this increase was 0.8 to 4.4% (all p less than 0.01). At 0.5 g/kg, and also at higher doses, there was a significantly (p less than 0.01) increased variance in RRL 8 to 16 min post-ethanol. A marked correspondence between mean RRL and ataxia is apparent. This appears to be the first in vivo demonstration of acute effects of ethanol on neuromuscular transmission. The methods and mice used may comprise a useful animal model for detecting acute effects of low doses of ethanol on synaptic function.

Excitability changes in peripheral nerve fibers after repetitive electrical stimulation

The Melzack-Wall gate control theory has been invoked to explain the peripheral analgesia resulting from repetitive electrical stimulation of peripheral nerve. This model emphasizes presynaptic inhibitory interactions among afferent fiber terminals in the spinal cord. An alternative explanation, that of velocity change in peripheral nerve fiber conduction, has been suggested by compound action potential studies from our laboratory. The present study was designed to extend this work, and to investigate the single fiber changes subsequent to brief (5- to 20-minute) periods of repetitive, high frequency (180 to 200/sec) electrical stimulation through an implantable peripheral nerve cuff device of the type used clinically for pain relief. Most fibers, regardless of their diameter (estimated from conduction velocity), show one or more of the following characteristics: a transient slowing of conduction velocity, an increase in electrical threshold and/or a decrease in response probability following a period of repetitive electrical stimulation. This supports the hypothesis that there are changes in direct peripheral nerve fiber excitability occurring under conditions simulating clinical electroanalgesia.

The effects of intra-arterial bradykinin, histamine, acetylcholine and prostaglandin E 1 on nociceptive and non-nociceptive dorsal horn neurones of the cat

The effects of peripherally administered algesic agents were investigated on the firing of cat dorsal horn interneurones classified as nociceptive or non-nociceptive according to the peripheral stimuli that excited them. A small amount of bradykinin injected into the blood supplying the receptive fields of cells was a potent specific stimulus causing activation of nociceptive cells and slowly conducting nerve fibres. Larger amounts of bradykinin and large amounts of histamine, 5-hydroxytryptamine and acetylcholine activated both nociceptive and non-nociceptive cells. Prostaglandin E 1 enhanced the effects of bradykinin and histamine on nociceptive cells. Prostaglandin E 1 also increased the response of these cells to the application of noxious heat whilst aspirin reduced this response. These results support a chemosensitive theory of nociceptor activation and show bradykinin to be the most potent and specific of the suggested endogenous algesic agents in causing activation of CNS nociceptive pathways.

Nerve fiber conduction-velocity distributions. II. Estimation based on two compound action potentials

A method is presented for estimating nerve fiber conduction velocity distributions from non-ivasive measurements of the compound action potential at two distinct locations separated by a known distance along the nerve bundle. This method is based on a model of the compound action potential as a weighted sum of delayed single-fiber action potential, but does not require explicit knowlege of the single-fiber action potential wave shapes in order to yield a unique estimate of the conduction velocity distribution. Illustrative examples are presented from normal and diseased nerves. This method appears to have clinical applications in the electrophysiological assessment of peripheral nerve function.

Exteroceptive vibration-induced finger flexion reflex in man.

A tonic finger flexion reflex, induced by mechanical vibration (100 Hz) of the fingers, was studied in 20 healthy subjects. The outcome of nerve blocking experiments indicated that the reflex is mainly exteroceptive, distinct from the tonic vibration reflex of muscle spindle origin. Mechanoreceptors with fast conducting nerve fibres in the distal phalanx seem to constitute the major afferent source. We suggest that afferent signals from such receptors by a feedback mechanism can influence the motor performance of the exploring fingers.

Neurophysiological effects of prolonged cooling of the calf in patients with complete spinal transection.

The neurophysiological effects of prolonged cooling were examined in seven patients with complete spinal lesions. The twitch tension of the soleus muscle, the direct (M-wave) and relfex (H-wave) response to electrical stimulation of the popliteal nerve, the Achilles tendon reflex (ATR) and the degree of inhibition of the H-wave by muscle vibration were recorded before and after a minimum of forty-five minutes cooling of the calf. Changes in the configuration of the M-wave occurred, suggesting that cooling results in slowing of conduction in muscle or motor nerve fibers. Prolongation of the twitch contraction and half relaxation time was observed, implying that the contractile mechanism of the muscle is affected. A significant decrease in the ATR/M ratio was observed, indicating that cooling, in addition, affects the muscle spindle or its connections. No significant alterations in the H/M ratio or in the degree of suppression of the H-wave by vibration were observed.

New Developments in Electromyography and Clinical Neurophysiology. Volume 1 New Concepts of the Motor Unit, Neuromuscular Disorders, and Electromyographic Kinesiology.John E. DesmedtNew Development in Electromyography and Clinical Neurophysiology. Volume 2: Pathological Conduction in Nerve Fibres, Electromyography of Sphincter Muscles, Automatic Analysis of Electromyogram with Computers.John E. DesmedtNew Development in Electromyography and Clinical Neurophysiology. Volume 3: Human Reflexes, Pathophysiology of Motor

Previous articleNext article No AccessNew Biological Books John E. Desmedt John E. Desmedt New Developments in Electromyography and Clinical Neurophysiology. Volume 1 New Concepts of the Motor Unit, Neuromuscular Disorders, and Electromyographic Kinesiology. John E. Desmedt New Development in Electromyography and Clinical Neurophysiology. Volume 2: Pathological Conduction in Nerve Fibres, Electromyography of Sphincter Muscles, Automatic Analysis of Electromyogram with Computers. John E. Desmedt New Development in Electromyography and Clinical Neurophysiology. Volume 3: Human Reflexes, Pathophysiology of Motor Systems, Methodology of. Human Reflexes. , John E. Desmedt Bentley GlassBentley Glass Search for more articles by this author PDFPDF PLUS Add to favoritesDownload CitationTrack CitationsPermissionsReprints Share onFacebookTwitterLinkedInRedditEmail SectionsMoreDetailsFiguresReferencesCited by The Quarterly Review of Biology Volume 49, Number 4Dec., 1974 Published in association with Stony Brook University Article DOIhttps://doi.org/10.1086/408278 Views: 1Total views on this site PDF download Crossref reports no articles citing this article.

The effect of cold on nerve conduction of human slow and fast nerve fibers

The effect of cold on nerve conduction of human slow and fast nerve fibers

Lateral line input to the crista cerebellaris in the eel. Field potentials and histology.

AbstractThe central nervous effects of electrical stimulation of the Nn. lat. posteriores have been investigated. Maximal field potential amplitudes were found in the medial part of the ipsilateral crista cerebellaris. The field potential evoked from stimulation of fast conducting nerve fibres consisted of an afferent pre‐synaptic volley and a post‐synaptic complex wave. The latter is shown to consist of a population EPSP and a population spike in subcristal neurones. Excitatory activity from the contralateral nerve impinges on the same neurones, and bilateral summation occurs. The contralateral field potential reverses more superficially than does the ipsilateral field. Post‐excitatory reduction of population spike can be explained by refractoriness. The crista region was investigated with conventional light and electron microscopical methods. Myelinated primary afferent axons from the R. lat post. N. X. terminate in the subcristal region on the ipsilateral side. Subcristal cells have dendritic ramifications in the molecular layer. Unmyelinated axons in this layer partly consist of lateral line primary afferents. These axons differ from the cerebellar parallel fibres by their extensive branching and irregular directional architecture. Fusiform swellings of these axons establish abundant isomorphous synapses with dendritic spines. The distribution of field potential negativity in depth corresponds to the distribution of subcristal neurones.

Effects of non-narcotic analgesics and nonsteroid anti-inflammatory agents upon inorganic phosphates, intracellular potassium and impulse conduction in mammalian nerve fibers

The effects of non-narcotic analgesics and of nonsteroid anti-inflammatory agents on the action potential and the content of intracellular potassium (K 1) and inorganic phosphate (P 1) were studied in the isolated cervical vagus nerve of the rabbit. Acetanilid, phenacetin and antipyrine in concentrations up to 10 mM showed no effect after incubations of 90 min at 37°. On the other hand, the anti-inflammatory agents, salicylic acid, phenylbutazone, oxyphenylbutazone, mefenamic, flufenamic and niflumic acid, in concentrations corresponding to the therapeutic level in human plasma during anti-rheumatic therapy, slowed nervous conduction and finally abolished excitability; this effect was accompanied by a loss of K 1 and an increase in P 1. Acetylsalicylic acid was ineffective at concentrations up to 5 mM, and abolished the action potential to 10 mM. Benzydamine, an anti-inflammatory agent without antirheumatic properties, abolished the action potential without elevation in P 1; barbituric acid, furosemide and the complexing agents, cysteamine, d-penicillamine and rubeanic acid, were ineffective. It is concluded that the abolition of excitability observed for the anti-inflammatory agents is due to the K 1 loss brought about by interference with oxydative phosphorylation. This effect does not appear to be due to their complexing action on metal ions.

Effects of salicylic and acetylsalicylic acid on inorganic phosphates and impulse conduction in mammalian nerve fibres.

Salicylic acid at therapeutic, and acetylsalicylic acid at higher concentrations, applied to desheathed rabbit vagus nerves in vitro, were found to increase the content in inorganic phosphates and to block conduction in both B-and C-fibres. The block developed slowly during incubation and was probably caused by an inhibitory effect on oxidative phosphorylation. Measurements of the salicylic acid content of the acetylsalicylic acid solution suggest that the action of acetylsalicylic acid was due to salicylic acid formed by hydrolysis.

Mechanism of cardiovascular action of tetrodotoxin in the cat. Block of conduction in peripheral sympathetic fibers.

Tetrodotoxin given to cats in doses of 1 to 10 µg/kg iv caused profound cardiovascular depression characterized by decreases in systolic and diastolic blood pressures, pulse pressure, heart rate, force of myocardial contraction, cardiac output and peripheral resistance. These effects were associated with marked inhibition of the responses to stimulation of nerves to the adrenal medulla and the sympathetic nerves to heart and blood vessels. Sinus bradycardia due to toxin did not occur after acute cardiac sympathetic denervation. In isolated sympathetic nerve-right atrium preparations, tetrodotoxin at 1 to 2 x 10 -8 g/ml abolished the positive inotropic and chronotropic responses to nerve stimulation without effect on spontaneous rate or force, or transmitter release by tyramine. Toxin-produced vasodilation in perfused hindlimbs was associated with marked inhibition of the normal vasoconstrictor responses to sympathetic vasomotor nerve stimulation. Vasodilation was not due to a direct action on vascular smooth muscle, since it was not seen after α-receptor blockade with phenoxybenzamine, after sympathetic denervation, or after blockade of adrenergic transmitter release by guanethidine or β-TM 10 accompanied by adrenalectomy. Vasodilators such as acetylcholine, histamine and isoproterenol consistently produced additional vasodilation under these conditions. The hypotensive effect of the toxin was also observed in spinal cats. It is concluded that the potent hypotensive action of tetrodotoxin, in the cat, is primarily due to blockade of conduction in peripheral sympathetic nerves and nerve fibers innervating the adrenal medulla.