CONDUCTION BLOCK OF TERMINAL SOMATIC MOTOR FIBERS IN TICK PARALYSIS

1960 ◽  
Vol 38 (1) ◽  
pp. 287-295 ◽  
Author(s):  
Maurice F. Murnaghan
Keyword(s):  
Motor Nerve ◽  
Conduction Block ◽  
Nerve Impulse ◽  
Nerve Fibers ◽  
Treated Animal ◽  
Direct Stimulation ◽  
High Potassium ◽  
Control Value ◽  
Choline Acetylase ◽  
Stimulation Of

In the perfused anterior tibial muscle of the tick-paralyzed dog acetylcholine in excess of the control value is not liberated on stimulation of the peroneal nerve; in the normal muscle 7 μμg of acetylcholine is liberated per nerve volley. The paralysis is evidently not due to defective synthesis of acetylcholine because acetylcholine is liberated in control and high-potassium perfusates, the choline acetylase activity and the acetylcholine content of lumbar ventral roots and peroneal nerves do not differ from that in normal dogs, and the tick-paralyzed muscle differs from that in the hemicholinium-treated animal in its response to a train of nerve pulses after previous tetanization. As somatic motor nerve fibers in the paralyzed dog have previously been shown to conduct a nerve impulse and the factors required for acetylcholine release at the nerve terminal apparently are not absent in the paralyzed animal, the mechanism of the paralysis is probably due to an inability of the nerve impulse to traverse the terminal presynaptic fibers. The 'lesion' evidently extends to the end of the presynaptic fiber, i.e. more distally than in botulism, because direct stimulation of the tick-paralyzed muscle fails to liberate acetylcholine.

CONDUCTION BLOCK OF TERMINAL SOMATIC MOTOR FIBERS IN TICK PARALYSIS

1960 ◽  
Vol 38 (3) ◽  
pp. 287-295 ◽  
Author(s):  
Maurice F. Murnaghan
Keyword(s):  
Motor Nerve ◽  
Conduction Block ◽  
Nerve Impulse ◽  
Nerve Fibers ◽  
Treated Animal ◽  
Direct Stimulation ◽  
High Potassium ◽  
Control Value ◽  
Choline Acetylase ◽  
Stimulation Of

In the perfused anterior tibial muscle of the tick-paralyzed dog acetylcholine in excess of the control value is not liberated on stimulation of the peroneal nerve; in the normal muscle 7 μμg of acetylcholine is liberated per nerve volley. The paralysis is evidently not due to defective synthesis of acetylcholine because acetylcholine is liberated in control and high-potassium perfusates, the choline acetylase activity and the acetylcholine content of lumbar ventral roots and peroneal nerves do not differ from that in normal dogs, and the tick-paralyzed muscle differs from that in the hemicholinium-treated animal in its response to a train of nerve pulses after previous tetanization. As somatic motor nerve fibers in the paralyzed dog have previously been shown to conduct a nerve impulse and the factors required for acetylcholine release at the nerve terminal apparently are not absent in the paralyzed animal, the mechanism of the paralysis is probably due to an inability of the nerve impulse to traverse the terminal presynaptic fibers. The 'lesion' evidently extends to the end of the presynaptic fiber, i.e. more distally than in botulism, because direct stimulation of the tick-paralyzed muscle fails to liberate acetylcholine.

ATP concentrations and muscle tension increase linearly with muscle contraction

2003 ◽  
Vol 95 (2) ◽  
pp. 577-583 ◽  
Author(s):  
Jianhua Li ◽  
Nicholas C. King ◽  
Lawrence I. Sinoway
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Motor Nerve ◽  
Muscle Tension ◽  
Nerve Fibers ◽  
Ventral Root ◽  
Ventral Roots ◽  
Root Stimulation ◽  
Stimulation Of

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636–H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 ± 2 and 16 ± 3 mmHg ( P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% ( P < 0.05) and 200% ( P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.

Short-range stiffness of slow fibers and twitch fibers in reptilian muscle

1976 ◽  
Vol 231 (2) ◽  
pp. 449-453 ◽  
Author(s):  
U Proske ◽  
PM Rack
Keyword(s):  
Short Range ◽  
Motor Nerve ◽  
Nerve Fibers ◽  
Repetitive Stimulation ◽  
Fiber Types ◽  
Cross Links ◽  
Stimulation Of Nerve ◽  
Limiting Value ◽  
Stimulation Of

The semitendinous muscle of the lizard Tilique contains both slow and twitch fibers; by subdivision of its motor nerve, fibers of each type may be stimulated separately. When, during repetitive stimulation of nerve filaments, the muscle was lengthened or shortened, the tension changes included an initial short-range stiffness, followed by a later compliance. With increasing velocities of movement, the short-range stiffness increased toward a limiting value. For slow fibers this limiting value was reached with lower velocities of movement than for the twitch fibers. Provided that the same velocity of movement was used and the movements began from similar initial isometric tensions, the slow fibers resisted the movements with a greater stiffness than the twitch fibers. It is suggested that not all of the observed differences between the two fiber types can be interpreted simply in terms of differences in rates of formation and breakdown of cross-links.

Bupivacaine Preferentially Blocks Ventral Root Axons in Rats

1997 ◽  
Vol 86 (1) ◽  
pp. 172-180 ◽  
Author(s):  
Friederike B. Dietz ◽  
Richard A. Jaffe
Keyword(s):  
Motor Nerve ◽  
Conduction Block ◽  
Sensory Nerve ◽  
Differential Susceptibility ◽  
Nerve Fibers ◽  
Ventral Root ◽  
Differential Sensitivity ◽  
Male Rats ◽  
Spinal Root

Background Clinically, bupivacaine can provide excellent sensory anesthesia with minimal impairment of motor function. However, the mechanisms by which local anesthetics produce differential sensory-motor nerve block is still unknown. The primary site of action for spinal and epidural anesthetics is thought to be the intradural segment of the spinal root. To determine the differential susceptibility of single motor and sensory nerve fibers to local anesthetic conduction block, bupivacaine effects on individual dorsal root (DR) and ventral root (VR) axons were studied. Methods Lumbar DRs and VRs were excised from anesthetized adult male rats. Single-fiber dissection and recording techniques were used to isolate activity in individual axons. Supramaximal constant-voltage stimuli at 0.3 Hz were delivered to the root. During in vitro perfusion, each root was exposed to increasing concentrations of bupivacaine, and the minimum blocking concentration (C(m)) and the concentration that increased conduction latency by 50% (latency EC50) were measured. Results Ventral root axons were significantly more sensitive to the steady-state conduction blocking effects of bupivacaine than were either myelinated or unmyelinated DR axons (DR-C(m), 32.4 microM; VR-C(m), 13.8 microM; P &lt; 0.0001). In addition, VR axons were more susceptible to the latency-increasing effects of bupivacaine than were DR axons (DR-EC50 = 20.7 microM; VR-EC50 = 8.5 microM; P &lt; 0.0001). Within axon groups, differential sensitivity as a function of conduction velocity (axon diameter), or length of nerve exposed to the anesthetic could not be demonstrated. Conclusions In contrast to clinical expectations, low concentrations of bupivacaine preferentially block motor (VR) axons in the rat.

scholarly journals The effect of muscular contraction upon the blood flow in the skeletal muscle, in the diaphragm and in the small intestine

1934 ◽  
Vol 114 (788) ◽  
pp. 245-257 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Motor Nerve ◽  
Muscular Contraction ◽  
Muscle Fibres ◽  
Direct Stimulation ◽  
Direct Excitation ◽  
Previous Communication ◽  
Arterial Inflow ◽  
Stimulation Of

In the previous communication, p. 233, experiments were described dealing with the effect of contraction of the skeletal muscle upon its blood flow. Short and prolonged tetanic contractions were evoked in various skeletal muscles by stimulation of their cut or uncut motor nerve or by direct stimulation of the muscle. Stimulation of the motor nerve as well as that of the muscle ma involve to an unknown extent the vasomotor innervation of the respective muscles and, although strong evidence was provided that none of the effects observed were even in part due to a direct excitation of the vasomotor fibres, we thought it necessary to repeat our experiments under conditions in which direct excitation of vasomotor fibres is definitely avoided. The present communication describes experiments on the reflex contraction of the tibialis and of the quadriceps femoris (vastocrureus) muscles. So far as we are aware, there is only one reference in the literature which related to circulatory conditions in muscles during a reflex contraction. Denny-Brown (1929), by direct microsopical observations of the surface of the soleus muscle during a stretch reflex, noticed that even a modest amount of pull on the tendon opens up numerous capillaries and hastens the flow of blood in them to a remarkable extent. The tension developed was sometimes as great as 1∙5 kg. Weight. As a result of this observation, Denny-Brown believes that the capillaries are not compressed by the muscle fibres when these contract reflexly. It is, however, quite likely that the circulatory conditions in the superficial layers of the muscle differ from those in the depth of the muscle. Moreover, it is extremely difficult to remove completely all the connective tissue from the surface of the muscle, and we know from Rein's experiments (Keller, Loeser, and Rein, 1930), as well as from our own previous experiments (Anrep, Blalock, and Samaan, 1933), that during the contraction of a muscle there may be considerable dilatation in the resting tissues. In order to determine the total arterial inflow into the tibialis anticus during its reflex contraction, we performed experiments which were similar to those described in our previous communication.

Monitoring of Spinal Cord Stimulation Evoked Potentials during Thoracoabdominal Aneurysm Surgery

Neurosurgery ◽  
1991 ◽  
Vol 28 (2) ◽  
pp. 325-330 ◽  
Author(s):  
Richard B. North ◽  
Benjamin Drenger ◽  
Charles Beattie ◽  
Robert W. McPherson ◽  
Stephen Parker ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Evoked Potentials ◽  
Evoked Potential ◽  
Conduction Block ◽  
Significant Risk ◽  
Thoracoabdominal Aneurysm ◽  
Direct Stimulation ◽  
Lower Extremity Ischemia ◽  
Extremity Ischemia ◽  
Stimulation Of

Abstract Repair of a thoracoabdominal aneurysm involves a significant risk of ischemic injury to the spinal cord. Standard monitoring of somatosensory evoked potentials, which relies upon peripheral nerve stimulation, becomes nonspecific and insensitive during this surgery when aortic cross-clamping produces lower extremity ischemia causing a peripheral conduction block. Techniques for the insertion of percutaneous epidural electrodes, developed originally for pain management, have been adapted to this setting to permit direct stimulation of the spinal cord for intraoperative monitoring of evoked potentials. The clinical outcome in patients monitored by this technique has been consistent with evoked potential findings.

scholarly journals MECHANISMS OF BIOELECTRIC ACTIVITY IN ELECTRIC TISSUE

1953 ◽  
Vol 37 (1) ◽  
pp. 91-110 ◽  
Author(s):  
Mario Altamirano ◽  
Christopher W. Coates ◽  
Harry Grundfest ◽  
David Nachmansohn
Keyword(s):  
Critical Size ◽  
Electrical Response ◽  
Electric Organ ◽  
Spatial Summation ◽  
Nerve Fibers ◽  
Direct Stimulation ◽  
Low Frequencies ◽  
Spike Discharge ◽  
High Frequencies ◽  
Stimulation Of

1. A preparation is described consisting of one or several layers of innervated cells of the electric organ of Electrophorus electricus. 2. Each plaque is multiply innervated and only at its caudal face. The nerve fibers may derive from two or more different nerve trunks. 3. During activity the innervated face becomes negative relative to the non-innervated. 4. The first electrical response of the cell to an increasing neural volley is graded and has the character of a prepotential. At a critical size of the prepotential the cell discharges with an all-or-nothing spike. 5. Both responses have durations of about 2 msec. 6. A neural volley which does not cause the spike discharge facilitates the discharge of the cell by a second subsequent volley in the same nerve (temporal facilitation). 7. The period of facilitation lasts ca. 900 msec. During the first 100 msec., the facilitation is large enough to cause a spike. In the later portion only the prepotential is facilitated. No electrical concomitant has been detected. 8. Neural volleys reaching the plaque from different trunks interact at the cell to produce a period of facilitation lasting only about 2 msec. This interaction is interpreted as spatial summation. 9. In a population of cells, simultaneous stimulation of 2 nerves causes a smaller discharge than the sum of the two isolated responses (occlusion). 10. Cells denervated for 7 weeks or more can be excited directly, but only by a current flow outward through the caudal face. 11. Weak direct stimulation causes a prepotential in the denervated plaque. On increasing the stimulus the prepotential increases to a critical size when a spike develops. The duration of both responses is about 2 msec. 12. The absolutely refractory period of the denervated cell is about 1.5 msec. and relative refractoriness lasts about 15 msec. 13. Direct stimulation causes slight facilitation lasting as long as 200 msec. 14. Repetitive stimulation of the nerve at low frequencies (2 to 3 per second) causes rapid "fatigue" of transmission. The denervated plaque, however, responds for several minutes to repetitive direct stimulation at high frequencies (25 per second).

scholarly journals The Electrodiagnosis of Ulnar Nerve Entrapment at the Elbow

2003 ◽  
Vol 30 (4) ◽  
pp. 314-319 ◽  
Author(s):  
Ralph Z. Kern
Keyword(s):  
Ulnar Nerve ◽  
Nerve Conduction ◽  
Motor Nerve ◽  
Conduction Block ◽  
Anatomical Variations ◽  
Nerve Fibers ◽  
Motor Nerve Conduction Velocity ◽  
Nerve Entrapment ◽  
Abductor Digiti Minimi ◽  
Nerve Dysfunction

Entrapment of the ulnar nerve at the elbow is the second most common focal peripheral neuropathy. Recent advances have facilitated the electrodiagnosis of this common nerve entrapment. The goals of electrodiagnosis are to localize ulnar nerve dysfunction, confirm that the disturbance is confined to the ulnar nerve, and assess the severity of ulnar nerve dysfunction. The goal of this review is to highlight the important advances in anatomy, neurophysiology and methodology that impact upon the electrodiagnosis of entrapment of the ulnar nerve at the elbow, illustrate the limits of electrodiagnosis, and discuss methodological issues that may be the subject of further study. Careful attention to elbow position, temperature, and conservative estimates of conduction block should be part of common practice. Awareness of anatomical variations in structural anatomy, anomalous innervation and fascicular arrangement of ulnar nerve fibers are required to interpret electrodiagnostic studies accurately. The most reliable finding is slowing of the ulnar across-elbow motor nerve conduction velocity to less than 50 m/sec while recording from the abductor digiti minimi muscle, and should be carefully interpreted in the presence of a polyneuropathy or other neurogenic process. Alternative techniques such as relative ulnar slowing in different ulnar nerve segments, use of alternative muscles, sensory and mixed nerve techniques provide complementary information, and like all nerve conduction studies are highly operator-dependent and should be used on a case by case basis. Recent studies have focused the electromyographer's attention on the use of shorter across-elbow segments (2-5 cm). This may offer a reasonable trade-off between sensitivity and measurement error and may result in improved electrodiagnosis.

scholarly journals The actions of eserine-like compounds upon frog’s nerve-muscle preparations, and the blocking of neuromuscular conduction

1940 ◽  
Vol 129 (856) ◽  
pp. 392-411 ◽  
Keyword(s):  
Neuromuscular Transmission ◽  
Motor Nerve ◽  
Calcium Content ◽  
Recovery Process ◽  
Direct Stimulation ◽  
Rate Of Recovery ◽  
Nerve Muscle ◽  
Minimum Interval ◽  
Site Of Stimulation ◽  
Stimulation Of

The actions of prostigmine, eserine, and the dimethylcarbamic ester of 8-hydroxymethylquinolinium methylsulphate upon the frog's isolated nervesartorius preparation have been examined by a method developed by Lucas (1911). With Ringer-soaked preparations from frogs kept at 14-18°C for some days before use the minimum interval at which two shocks applied to the nerve could elicit a summated muscular response was about 20% longer than the absolute refractory period of the nerve. Any of the above-mentioned compounds prolonged the minimum interval for a summated response, but caused the time at which an extra interpolated shock began to cut down the response to the final shock to become only a little later. Curarine or atropine reversed the prolongation of minimum interval. By the same method, the actions of the same eserine-like compounds upon preparations which had been treated with Ringer's solution of half the usual calcium content were examined. Either before or after treatment, it was impossible to cut down the muscular response by interpolating an extra shock. The action of prostigmine upon Ringer-soaked preparations was examined by a method developed by Adrian (1913), involving determination of the rate of recovery of excitability in the motor nerve at the site of stimulation and in the remaining more peripheral part of the preparation. Prostigmine influenced little the recovery process at the site of stimulation, whereas it prolonged the slower and more peripheral recovery process. Curarine reversed the prolongation of the more peripheral recovery. With Ringer-soaked preparations, during the block of neuromuscular transmission produced by rapid repetitive stimulation of the nerve, the response of the muscle to direct stimulation was reduced. If, however, neuromuscular transmission had been blocked by curarine, stimulation of the nerve did not reduce the response of the muscle to direct stimulation.

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