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At least 19 recordsLinked to original sources

PubMed1977

The declining electrical response of muscle to repetitive nerve stimulation in myotonia.

The electrical response of muscle to repetitive nerve stimulation was studied in patients with various myotonic disorders. A decrementing response was common but not invariable finding, and was unrelated to the severity or diagnosis. The decrement either continued throughout the period of stimulation or "leveled off", sometimes being followed by an increment. If it occurred at low rates of stimulation, a greater decrement occurred at higher rates, usually after a shorter latent period. It was not related consistently to the presence of weakness, but in patients with myotonia congenita it was more conspicuous and elicited by lower rates of stimulation when transient weakness was a feature of the history.

Adolescent↗

PubMed1975

Guanidine and neuromuscular transmission. II. Effect on transmitter release in response to repetitive nerve stimulation.

The effect of guanidine on the neuromuscular transmission in human intercostal and mouse diaphragm muscle in vitro during repetitive nerve stimulation was studied. The drug greatly increased the release of acetylcholine (ACh) quanta by nerve impulses at low frequencies of nerve stimulation and at the beginning of tetani at high frequencies of stimulation. The effect was shown to be produced by an increase in fractional release from an unchanged store of ACh quanta available fro immediate release. This seems to explain why guanidine has a poor therapeutic effect in myasthenia gravis but a good effect in the myasthenic syndrome.

Acetylcholine↗

PubMed1977

Afterdischarge on postganglionic sympathetic nerves following repetitive stimulation of the preganglionic nerve to the rat superior cervical ganglion in vitro.

An asynchronous firing or afterdischarge (AD) was recorded in vitro from the postganglionic internal carotid nerve of the rat superior cervical ganglion following repetitive stimulation of the preganglionic nerve when ganglion transmission was blocked by chlorisondamine, nicotine or hexamethonium, but was rarely observed in untreated ganglia. A stimulus frequency of at least 5 Hz was required to induce AD and as few as 100 pulses caused a significant response. The amplitude and duration of AD varied with the number of pulses. Low calcium solutions resulted in AD in the absence of ganglion blocking drugs, and high calcium solutions or low concentrations of atropine abolished the AD. Increasing magnesium concentration to 10 mM or the manganese concentration to 0.1 mM reduced or prevented AD following preganglionic nerve stimulation. The onset of AD was delayed in potassium-free solutions and at a lowered temperature. Dinitrophenol had a small depressant effect on AD but sodium azide reduced the amplitude significantly. Exposure of ganglia to bethanechol, 300 to 600 muM, resulted in asynchronous firing recorded from postganglionic nerves, and stimulation of the preganglionic nerve transiently depressed the drug-induced firing but enhanced the firing 30 to 60 seconds after the volley. Physostigmine did not alter the amplitude of bethanechol-induced firing after a volley. Prolonged high frequency (40 Hz) stimulation of the preganglionic nerve increased the AD following a 20 Hz test volley for up to 1 hour. It is concluded that increasing the release of acetylcholine or blockade of nicotinic receptors makes more acetylcholine available for interaction with muscarinic receptors, and that stimulation of the preganglionic nerve unmasks or sensitizes ganglionic muscarinic receptors. No clear evidence of a metabolic basis for the muscarinic response was obtained.

Animals↗

PubMed1976

Pathological mechanisms in experimental autoimmune myasthenia gravis. II. Passive transfer of experimental autoimmune myasthenia gravis in rats with anti-acetylcholine recepotr antibodies.

Passive transfer of experimental autoimmune myasthenia gravis (EAMG) was achieved using the gamma globulin fraction and purified IgG from sera of rats immunized with Electrophus electricus (eel) acetylcholine receptor (AChR). This demonstrates the critical role of anti-AChR antibodies in impairing neuromuscular transmission in EAMG. Passive transfer of anti-AChR antibodies from rats with chronic EAMG induced signs of the acute phase of EAMG in normal recipient rats, including invasion of the motor end-plate region by mononuclear inflammatory cells. Clinical, eletrophysiological, histological, and biochemical signs of acute EAMG were observed by 24 h after antibody transfer. Recipient rats developed profound weakness and fatigability, and the posture characteristic of EAMG. Striking weight loss was attributable to dehydration. Recipient rats showed large decreases in amplitude of muscle responses to motor nerve stimulation, and repetitive nerve stimulation induced characteristic decrementing responses. End-plate potentials were not detectable in many muscle fibers, and the amplitudes of miniature end-plate potentials were reduced in the others. Passively transferred EAMG more severely affected the forearm muscles than diaphragm muscles, though neuromuscular transmission was impaired and curare sensitivity was increased in both muscles. Some AChR extracted from the muscles of rats with passively transferred EAMG was found to be complexed with antibody, and the total yield of AChR per rat was decreased. The quantitative decrease in AChR approximately paralleled in time the course of clinical and electrophysiological signs. The amount of AChR increased to normal levels and beyond at the time neuromuscular transmission was improving. The excess of AChR extractable from muscle as the serum antibody level decreased probably represented extrajunctional receptors formed in response to functional denervation caused by phagocytosis of the postsynaptic membrane by macrophages. The amount of antibody required to passively transfer EAMG was less than required to bind all AChR molecules in a rat's musculature. The effectiveness of samll amounts of antibody was probably amplified by the activation of complement and by the destruction of large areas of postsynaptic membrane by phagocytic cells. A self-sustaining autoimmune response to AChR was not provoked in animals with passively transferred EAMG.

Animals↗

PubMed1978

Changes in extracellular potassium during the spontaneous activity of medullary respiratory neurones.

In 34 cats, the changes in extracellular potassium ion activity (aK) and extracellular spike activity within the pool of respiratory neurones in the dorsormedial and ventrolateral medulla were recorded using microelectrodes filled with a liquid potassium ion exchange resin. Cyclic changes in aK which parallel central respiratory activity were restricted to those regions where respiratory neurones are known to be localized. The largest changes in aK (0.1--0.3 mmol . 1(-1)) were found within the ventral pool of inspiratory neurones. The aK increased during inspiration in parallel with the pattern of phrenic nerve activity. The smallest changes in aK (0.02--0.06 mmol . 1(-1)) were observed within the ventral pool of expiratory neurones. Here, aK showed a transient increase during both inspiration and expiration. Within the dorsal pool of inspiratory neurones, small fluctuations of aK were observed paralleling phrenic nerve activity and the afferent discharge of the intact vagal nerves. After the vagal nerves were cut, the changes in aK then paralleled phrenic nerve activity. The variations in aK within the ventral pool of respiratory neurones did not change after bilateral section of vagal nerves. Repetitive stimulation of the vagal nerves (0.1--0.5 V, 0.05 ms) produced an increase in aK only within the dorsal pool of inspiratory neurones, whereas repetitive spinal cord stimulation (5--10 V, 0.05 ms) resulted in an increase of aK within the ventral pool of respiratory neurones. The amplitude of the cyclic changes in aK increased significantly whenever the electrode approached individual respiratory neurones as verified by the amplitude and shape of the spikes recorded by the reference barrel. The maximal changes in aK then reached a peak amplitude of 1.3--1.5 mmol . 1(-1), the pattern of aK changes resembling that measured within the pools of neurones. The aK started to rise prior to the discharge of action potentials, indicating that the efflux of K + -ions was produced as a consequence of synaptic transmission. The functional importance of these changes in extracellular potassium is discussed.

Animals↗

PubMed1977

Can barium support the release of acetylcholine by nerve impulses?

Conventional electrophysiological techniques were used to study the effects of Ba on the release of acetylcholine (ACh) from frog motor nerve terminals. Equimolar substitution of Ba for Ca eliminated end-plate potentials (e.p.ps) without a corresponding decline in the amplitude of the nerve terminal action potential. Miniature end-plate potentials (m.e.p.ps) were readily detectable in Ba solutions despite a depolarized muscle membrane. Studies on the e.p.p. in curarized preparations bathed with different concentrations of Ca and Ba suggest that Ba may compete with Ca in the process by which depolarization of the nerve terminal leads to the release of ACh. Repetitive nerve stimulation at 1 Hz in Ba solutions caused 5-20 fold increases in m.e.p.p. frequencies (7 experiments). Stimulation of Ba-bathed preparations at 10 Hz elevated m.e.p.p. frequencies to very high levels that could not be measured accurately (''100/s). It is suggested that the asynchronous discharge of m.e.p.ps produced by repetitive nerve stimulation is the electrophysiological correlate of the evoked ACh outflow in Ba solutions detected previously by bioassay of ther perfusion fluid.

Acetylcholine↗

PubMed1975

[Electrophysiology in neuropathy caused by vincristine].

Ten patients treated with vincristine were submitted for electrophysiological examination. It was investigated the number of motor units within the thenar muscle following a technique described previously (Sica et al. - 1974); motor and sensitive conduction velocities as well as motor distal latencies in the median nerve were studied following conventional techniques. The behaviour of the evoked muscle potential with repetitive supramaximal stimulation over the median nerve was also investigated. The findings were compared with control groups. The estimated number of motor units was disminished in eight of ten patients and the average number was significantly different from the control group (control 318 +/- 71 UM; patients 174 +/- 84 UM; P less than 0.001). The potential amplitudes in most of the surviving units were reduced, others remaining within the normal range. This makes apparent that the peripherical nervous system fails to compensate adequately and, furthermore, a loss of individual muscle fibres occurs within some individual units. The conduction velocities of the fastest conducting motor nerve fibres were reduced and motor distal latencies prolongued (Table 1). Maximal impulse conduction velocities were measured in sensory fibres. In 5 of 7 subjets investigated the values laied just beyond the lower limit of the normal range. The amplitude of the sensory orthodromic evoked potential in the median nerve at the wrist was disminished almost in the whole group. The decremental muscle response to repetitive nerve stimulation, can be interpreted as the result of the damage at the neural apparatus at the motor end plate; it was observed in 57% of the patients. In summary, evidences have been registered showing that the nervous supply to the muscle is affected in patients treated with vincristine; the motor unit behaviour under this conditions is discussed.

Adult↗

PubMed1977

Botulism: electrophysiological studies.

In a patient with botulism type B, electrophysiological studies showed: (1) a pattern in the repetitive nerve stimulation test resembling that found in the Eaton-Lambert syndrome but without any significant increment at high rates of stimulation or posttetanic exhaustion phenomenon; (2) a prominent response to guanidine hydrochloride; (3) a short mean duration of motor unit potentials that reversed with recovery; (4) a mild, prolonged latency and low amplitude of the H-reflex; (5) mild peripheral nerve dysfunction; and (6) a long-lasting persistence of abnormalities beyond the time of clinical recovery. The literature reports two types of responses in the repetitive nerve stimulation test in botulism: in the severe form one obtains a low-amplitude muscle potential, a decremental response at low rates of stimulation, and an insignificant incremental response at high rates of stimulation; in the mild form a normal amplitude of muscle potential occurs together with a normal response to low rates of stimulation and a significant incremental response at high rates of stimulation.

Botulism↗

PubMed1977

Clinical electromyography: definition, application, and innovation.

Clinical EMG techniques, useful in the study of patients with neuromuscular disease, are defined. These include measurement of motor and sensory nerve conduction velocities; analysis of the size, shape, and latency of response of muscle and nerve action potentials after nerve stimulation; estimates of nerve excitability; study of the response to repetitive nerve stimulation as a measure of neuromuscular transmission; and observation of the electrical activity of muscle with needle recording electrodes (monopolar, bipolar, and multielectrodes). From a consideration of the application, limitations, and value of these various techniques, it can be concluded logically that to assure the highest probability of reliable information in regard to an individual patient, the choice of technique(s) and the part(s) to be studied should be intimately tied to a clinical analysis of that patient's problem. EMG as a fishing expedition is rarely fruitful; EMG as an exercise in clinical physiology is often exciting.

Action Potentials↗

PubMed1978

4-Aminopyridine and evoked transmitter release from motor nerve endings.

1 In the presence of tetrodotoxin, electrotonic depolarization of frog motor nerve terminals causes the appearance of stimulus-graded endplate potentials. When 4-aminopyridine is added, the graded endplate potential is converted into a triggered all-or-none response resulting in giant endplate potentials of about 70 mV amplitude and 50 ms duration. The triggered endplate potentials are abolished in Ca(2+)-free saline and are blocked by Mn(2+) ions. Sr(2+) but not Ba(2+) can replace Ca(2+) in supporting transmitter release. Mg(2+) fails, even in concentrations as high as 32 mM, to affect the amplitude and the shape of the endplate potential but abolishes it when the Ca(2+) concentration is reduced to 0.2 mM.2 Despite the large amplitude of the triggered endplate potential in the presence of 4-aminopyridine and tetrodotoxin, repetitive stimulation up to 10 Hz causes only a small decline in amplitude of successive endplate potentials. However, in the presence of (+)-tubocurarine or gallamine, repetitive nerve stimulation produces a marked decline in successive endplate potential amplitude. The fall is counteracted when evoked transmitter release is reduced in the presence of 0.2 mM Ca(2+). The results suggest that in the presence of 4-aminopyridine such large amounts of transmitter are released that even during repetitive stimulation (5 to 10 Hz) endplate potentials are of maximal amplitude.3 4-Aminopyridine causes a prallel shift to the right of the dose-response curve to Mg(2+) for blockade of nerve impulse-evoked transmitter release (in the absence of tetrodotoxin). A similar parallel shift occurs in the presence of tetraethylammonium and guanidine.4 It is concluded that 4-aminopyridine increases transmitter release by enhancing the transport efficacy for Ca(2+) across the nerve terminal membrane during nerve terminal depolarization.

Aminopyridines↗

PubMed1978

Myotonia induced with clofibrate in rats.

Myotonia was induced in rats with clofibrate given in daily subcutaneous injections of 0.4 g/kg. The first myotonic discharges were recorded electromyographically from the extensor digitorum longus, tibialis anterior, and gastrocnemius muscles after 4 days on clofibrate, but from the soleus not until after 11 days. Clofibrate induced myotonic activity in chronically denervated muscle also. During repetitive nerve stimulation the electrical response of the muscle was declining in all myotonic rats. It did so also when repetitive stimulation was applied directly to the muscle, which would seem to suggest a myotonic defect as the cause. Several drugs were tested and diphenylhydantoin proved to inhibit myotonia most effectively. Animals on an extended clofibrate schedule (12 weeks) had ECG abnormalities resembling those seen in patients with myotonic dystrophy.

Action Potentials↗

PubMed1979

Depression, facilitation, and mobilization of transmitter at the rat diaphragm neuromuscular junction.

The characteristics of depression, facilitation, and mobilization of transmitter were examined at the rat diaphragm neuromuscular junction. Intracellular recording techniques were used to monitor end-plate potentials (EPPs), miniature end-plate potentials (MEPPs) and the muscle resting potentials. The cut-muscle technique was used to prevent muscle action potentials. Quantal release was determined by the direct method. The binomial statistical parameters, releasable store (n) and probability of release (p), were examined under various stimulating conditions to determine the basis for depression and facilitation. The present experiments demonstrate that p remains unchanged during repetitive nerve stimulation at low or moderately high frequencies. The experiments demonstrate that depression is due to a decrease in n and facilitation is due to an elevation in n. It is suggested that the increase in n during facilitation is due to a transient recruitment of inactive releasing sites. Substantial replenishment of n by mobilization occurs within a few ms after a stimulus but a slow residual rate of mobilization is needed to replenish n to resting levels.

Animals↗

PubMed1978

On the role of barium in supporting the asynchronous release of acetylcholine quanta by motor nerve impulses.

1. The effect of Ba2+ on the evoked secretion of individual acetylcholine (ACh) quanta was studied on frog neuromuscular junctions using conventional electro-physiological techniques. 2. In solutions containing 1.8 mM-Ba2+ and no added Ca2+, 1 Hz stimulation for less than 1 min elevated miniature end-plate potential (m.e.p.p.) frequencies to 5-20 times the control level (seven experiments). Similar results were obtained when a Ca2+-chelating agent was added to the Ba2+ solution. 3. Repetitive nerve stimulation at frequencies greater than 1 Hz in concentrations of Ba2+ greater than or equal to 1.8 mM elevated m.e.p.p. frequencies to unmeasurable levels (greater than 100/sec). Such high m.e.p.p. frequencies were accompanied by a steady depolarization of the post-synaptic membrane, which was used to estimate the number of ACh quanta released. 4. The number of ACh quanta released asynchronously by nerve impulses was directly related to the external concentration of Ba2+ in a non-linear fashion. 5. Ba2+ was two orders of magnitude more effective than Ca2+ in supporting the evoked discharge of m.e.p.p.s. Ca2+ was a potent antagonist of asynchronous release in Ba2+ solutions. 6. Mg2+ and Co2+ both competitively antagonized evoked release in Ba2+ solutions. The equilibrium dissociation constant for each ion as an antagonist of asynchronous, Ba2+-dependent release was similar to its corresponding value as an antagonist of synchronous, Ca2+-mediated release. 7. It is suggested that Ba2+ supports dispersed, quantal ACh release directly by acting through the same conductance pathway normally traversed by Ca2+.

Acetylcholine↗

PubMed1979

gamma-Aminobutyric acid efflux from sympathetic glial cells: effect of 'depolarizing' agents.

1. Isolated desheathed rat superior cervical ganglia were incubated in [3H]2,3,-gamma-aminobutyric acid ([3H]GABA) solution (1--10 microM for 2--3 hr) in the presence of 10 microM-amino-oxyacetic acid (AOAA). The subsequent efflux of tritium into a stream of superfused non-radioactive GABA-free Krebs solution at 25 degrees C was measured. 2. In the presence of 10 micrometer-AOAA the mean basal efflux rate coefficient (k0) for exit of tritium into the superfusion fluid was 0.7 x 10(-3) min-1. More than 98% of effluent tritium comprised unchanged [3H]GABA. The rate coefficient showed no correlation with the amount of [3H]GABA previously accumulated by the ganglion. 3. Elevation of [K+]o to greater than 50 mM increased the rate coefficient for [3H]GABA release by up to four times. Changes in efflux rate were not correlated with osmotic changes, and persisted after re-accumulation of effluent [3H]GABA by the inward carrier was inhibited. The effect of alkali metal cations diminished in the order Rb+ greater than K+ greater than Cs+Li+. Effects of K+ solutions were not reduced by omitting Ca2+ ions, with or without the addition of Mg2+. 4. Application of electrical pulses (0.1--1 msec duration, 1--10 Hz, 4 min trains) to the ganglion soma or to the preganglionic nerve trunk also raised k0. This effect declined with repeated stimulus trains, without an accompanying diminution in the response to K+. Responses to electrical stimulation were not reduced by amethocaine (300 microM), tetrodotoxin (3 microM) or raised [Mg2+i1 (0 mM-[Ca2+]/30 mM-[Mg3+]). Separate local superfusion of the pre- and post-ganglionic nerve trunks and of the ganglion soma showed that the response to electrical stimulation was localized to the vicinity of the stimulus and was not propagated along the nerve trunks or across the synapses. 5. Electrical recording from impaled 'inexcitable' cells (presumed to be neuroglial cells (Appendix)) indicated that the quantities of K+ ion accumulating during repetitive nerve stimulation are insufficient to stimulate the release of GABA from the glial cells. No physiological role for the release process in modulating neuronal excitability could be adduced.

Aminooxyacetic Acid↗

PubMed1978

Adrenergic and 'non-adrenergic' components in the contractile response of the vas deferens to a single indirect stimulus.

1. The mechanical response of the longitudinal smooth muscle of the rat vas deferens to stimulation of its motor nerves by a single pulse has been examined. The motor nerves were stimulated in vivo via the spinal outflows in the pithed rat or in vitro by field stimulation. 2. The contraction in the whole vas consisted of two components, an initial, rapid, brief contraction reaching a maximum at 300 msec and a second, slower and more prolonged contraction reaching its maximum at 600 msec. When the isolated vas was divided into prostatic and epididymal halves the contribution of these two components varied. The initial rapid component was more prominent in the prostatic half and the slower, second component more prominent in the epididymal half. Lowering the bath temperature caused, in both halves, these two components to merge into a single, slow, prolonged response. Both components were more rapid and briefer than the equivalent response of rat anococcygeus. 3. The second, slow component was abolished by alpha-adrenoceptor antagonist drugs, potentiated and prolonged by drugs which inhibit the neuronal uptake of noradrenaline and absent from tissues taken from rats pre-treated with reserpine, suggesting that the neurotransmitter for this component is noradrenaline. 4. These experiments were extended to the mouse or guinea-pig vas deferens. Both showed the same two component mechanical response as the rat vas and in both the second, slow component was preferentially inhibited by alpha-adrenoceptor antagonists and potentiated by drugs blocking noradrenaline uptake. 5. Drugs known to reduce the response to repetitive nerve stimulation of the vas were examined for their effect on the response to a single stimulus. Lysergic acid diethylamide preferentially inhibited the second, slow phase of contraction whereas apomorphine preferentially inhibited the first rapid phase. Guanethidine inhibited responses but any differential effects could not be analysed due to its stimulant properties. 6. These results show that there are two components even to the response to a single stimulus. The second of these appears to be adrenergic while the transmitter responsible for the first remains to be determined.

Adrenergic Fibers↗

PubMed1977

Acetylcholine receptor protein. Neuromuscular transmission in immunized rabbits.

Rabbits injected with purified acetylcholine (ACh) receptor protein produce antibodies against the receptor and develop generalized muscle weakness. The compound muscle action potentials show a decremental fall in amplitude with repetitive nerve stimulation. Both the weakness and the decrement is counteracted by reversible cholinesterase inhibitors. Intracellular recordings from muscle endplates show that the amplitude of the miniature end-plate potentials is considerably reduced. A reduced binding of neurotoxin to muscles from immunized rabbits was observed. Nerve impulses release a normal number of ACh packages (quanta) from the motor nerve terminals. The muscle weakness in immunized rabbits thus has the same features as the muscle weakness in myasthenia gravis and may be a good animal model of myasthenia gravis.

Acetylcholine↗

PubMed1977

Ocular involvement in wound botulism.

A 7-year-old girl developed bilateral ptosis, total ophthalmoplegia, and fixed, dilated pupils associated with bulbar paralysis and generalized weakness six days after she sustained a compound supracondylar fracture of the right humerus. Nerve conduction studies showed a facilitated muscle action potential after repetitive nerve stimulation. Blood cultures were negative. Although the wound site appeared noninfected, the wound was explored. Clostridium botulinum, type B, grew from cultures taken from the depths of the wound. The patient recovered fully with supportive care, and EEG abnormalities present during the acute phase of the illness disappeared.

Adolescent↗

PubMed1975

Clinical and electrophysiological observations in patients with myotonic muscle disease and the therapeutic effect of N-propyl-ajmalin.

Six patients with congenital myotonia and 4 patients with myotonic dystrophy have been examined clinically before and after the administration of N-propyl-ajmalin, an alkaloid frequently used as a cardiac antiarrhythmic drug. All patients but one reported a good to moderate improvement of their myotonic muscle stiffness. This was verified by measuring the time the patients needed to ascend a flight of stairs and by recording the speed of opening the hand. The amplitude of the compound muscle action potential decreased during repetitive nerve stimulation in myotonic patients. This decrease was not influenced by N-propyl-ajmalin. It seems to be due to the increased after-depolarization observed in myotonic fibres which causes partial inactivation of the Na-carrying system. From one patient a muscle biopsy was taken and intracellular potentials were measured with a microelectrode. Almost all muscle cells investigated showed myotonic activity which was completely abolished by addition of 10(-5) g/ml N-propyl-ajmalin to the bathing fluid. The development and duration of "warm-up" is illustrated and a possible electrophysiological basis is discussed.

Action Potentials↗