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Motor nerve stimulation, responses

Figure 1. Responses in the house fly dorsolongitudinal flight muscles to motor nerve stimulation. In this preparation, action potentials in the muscle faithfully reflect activity present in the motor neuron. (a) Control preparations respond to stimulation by firing a single muscle action potential. (b) Treatment with fenfluthrin initiates high frequency burst discharge from a single stimulus. Figure 1. Responses in the house fly dorsolongitudinal flight muscles to motor nerve stimulation. In this preparation, action potentials in the muscle faithfully reflect activity present in the motor neuron. (a) Control preparations respond to stimulation by firing a single muscle action potential. (b) Treatment with fenfluthrin initiates high frequency burst discharge from a single stimulus.
Quantal analysis defines the mechanism of release as exocytosis. Stimulation of the motor neuron causes a large depolarization of the motor end plate. In 1952, Fatt and Katz [11] observed that spontaneous potentials of approximately 1 mV occur at the motor endplate. Each individual potential change has a time course similar to the much larger evoked response of the muscle membrane that results from electrical stimulation of the motor nerve. These small spontaneous potentials were therefore called... [Pg.172]

Measuring muscle-evoked responses to repetitive motor nerve electrical stimulation permits detection of presyn-aptic neuromuscular junction dysfunction. In botulism and the Lambert-Eaton syndrome, repetitive stimulation elicits a smaller than normal skeletal muscle response at the beginning of the stimulus train, due to impaired initial release of acetylcholine-containing vesicles from presyn-aptic terminals of motor neurons followed by a normal or accentuated incremental muscle response during repeated stimulation. This incremental response to repetitive stimulation in presynaptic neuromuscular disorders can be distinguished from the decremental response that characterizes autoimmune myasthenia gravis, which affects the postsynaptic component of neuromuscular junctions. [Pg.620]

Sanders If you get rid of the interstitial cells there is no further response to nerve stimulation. You can get a nice response to acetylcholine. Then you go back to the wild-type animal and you can block the breakdown of acetylcholine and then get a smooth muscle response. The point is that while there are synaptic connections in GI smooth muscle, synaptic connections between the motor neurons and smooth muscles are not so common. The major synaptic connections are between the motor neurons and the interstitial cells. [Pg.79]

Figure 13.9 k soldier wounded at the Battle of Corunna (a battle in the Peninsular War) suffering simultaneous contraction of all muscles after infection with the bacterium, Clostridium tetani. Both agonist and antagonist muscles are active in this condition. The bacterium is found in the earth, especially in places where animal faeces have been present. Bacteria invade the body through a wound, especially in soldiers in battle. The bacterium secretes a toxin that is absorbed into the motor nerves which then become acutely responsive to mild stimuli. It can lead to death unless treated (from Bell 1824). The toxin is now used in cosmetic manipulation to stimulate contraction of muscles in the face to tighten the skin which removes or conceals wrinkles (Botox). [Pg.283]

Histamine is a powerful stimulant of nerve endings, both motor and sensory nerves (32). Its stimulation is important in producing pain and itching, which are important components of the urticarial response and reactions to insect stings ( ). This effect is mediated through Hj receptors. Such nerve stimulation might conceivably be important in the initiation of the emetic response. [Pg.427]

Monitoring the effect of muscle relaxants during surgery (and recovery following the use of cholinesterase inhibitors) typically involves the use of a device that produces transdermal electrical stimulation of one of the peripheral nerves to the hand and recording of the evoked contractions (twitches Figure 27-6). The motor responses to different patterns of peripheral nerve stimulation are measured. The three most commonly used patterns of include (1) single-twitch stimulation, (2) train-of-four (TOF) stimulation, and (3) tetanic stimulation. Two newer modalities are also available to monitor neuromuscular transmission double-burst stimulation and posttetanic count. [Pg.620]

Certain other substances (tetanus toxin) reach nerve cells directly via distal axonal entry. Tetanus toxin is transported to the spinal anterior horn cell, subsequently translocates and binds to presynaptic inhibitory (glycinergic) nerve terminals impinging on the motor nerve cell, and thereby suppresses the inhibition of motor neuron activity leading to hyperexcitation. Violent and sustained muscle contraction (tetany) results in response to external stimulation. Another example of peripheral entry to the CNS is the transport and delivery of metals (manganese, aluminum) from the nose along olfactory neurons to the brain of laboratory animals. [Pg.1793]

PHARMACOLOGY, TOXICOLOGY, AND DISPOSITION The reactivating action of oximes in vivo is most marked at the skeletal neuromuscular junction. Following a dose of an organophosphorus compound that produces total blockade of transmission, the intravenous injection of an oxime restores responsiveness of the motor nerve to stimulation within minutes. Antidotal effects are less striking at autonomic effector sites, and the quaternary ammonium group restricts entry into the CNS. [Pg.131]

A large number of methods has been used to demonstrate curare activity and to evaluate the materials which exhibit it. The abolition of response of muscle to electrical stimulation of motor nerves has been used as a qualitative determination of curare activity (13). One of the oldest methods for quantitative determinations is the intralymphal injection in frogs. The minimum dose required to cause complete paralysis is determined. Other animals (mice, rats, dogs, cats) have been used in complete paralysis experiments. The biggest disadvantage in using whole animals is that the site of the action is not readily discerned. [Pg.268]

The causative oiganophosphate was identified in nine patients four fenthion, two dimethoate. two monocrotophos, and one mclhamidophos. Standard biochemistry and cerebrospinal fluid examination were normal. Cholinesterase (ChE) assays were not available. Electromyography (EMG) showed normal motor and sensory nerve conduction velocities and normal needle myography. Tetanic stimulafion of the abductor pollicis brevis muscle 24-48 hr after the onset of IMS showed a marked fade at 20 and 50 Hz. A train of four stimuli applied at 2 Hz produced no changes in the amplitude of the compound muscle action potential (CMAP). CMAPs are the motor responses recorded with surface electrodes over a muscle after stimulation of its motor nerve. [Pg.371]

Barth6, L., and SzolcsAnyi, J., 1980, The mechanism of the motor response to periarterial nerve stimulation in the intestine of the rabbit, Br.J. Pharmacol. 70 193-195. [Pg.226]

Studies Acetylcholine receptor binding and blocking antibodies were positive, as was the anti-striated-muscle antibody. Other immunological parameters were normal, as were thyroid function tests. Repetitive nerve stimulation at low-frequency (3 Hz) showed an 18% decremental response of the compound-motor-unit potential indicating MG (normal is < 11 % decrement). Nerve conduction studies were normal. Computed tomography (with contrast) of the mediastinum revealed a mass, presumably thymoma. [Pg.62]


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See also in sourсe #XX -- [ Pg.203 ]




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