Muscle motor end plate

The somatic motor nervous system or voluntary nervous system consists of nerve libers that irmervate skeletal muscle motor end-plates. 

The action of acetylcholine at the skeletal muscle motor end plate resembles that produced by nicotine. Thus, the choUnoreceptor on skeletal muscle is a nicotinic receptor. Based on antagonist selectivity, however, the autonomic and somatic nicotinic receptors are not pharmacologically identical (see Chapter 14). 

Most of the direct organ system effects of muscarinic cholinoceptor stimulants are readily predicted from a knowledge of the effects of parasympathetic nerve stimulation (see Table 6-3) and the distribution of muscarinic receptors. Effects of a typical agent such as acetylcholine are listed in Table 7-3. The effects of nicotinic agonists are similarly predictable from a knowledge of the physiology of the autonomic ganglia and skeletal muscle motor end plate. 

The neuromuscular junction consists of a motor nerve terminal and skeletal muscle motor end plate, separated by a synaptic cleft that is filled with extracellular fluid (Figure 26.2). 

Nm—Nicotinic receptors are located on the skeletal muscle motor end plate innervated by somatic motor nerves. 

Electron microscopic study reveals an incalculably small space between nerve endings and the effector organ (eg, tlie muscle, cell, or gland) diat is innervated (or controlled) by a nerve fiber. Fbr a nerve impulse to be transmitted from die nerve ending (motor end plate) across die space to die effector organ, a neurohormone is needed. 

According to Fig. 6.17 the nerve cell is linked to other excitable, both nerve and muscle, cells by structures called, in the case of other nerve cells, as partners, synapses, and in the case of striated muscle cells, motor end-plates neuromuscular junctions). The impulse, which is originally electric, is transformed into a chemical stimulus and again into an electrical impulse. The opening and closing of ion-selective channels present in these junctions depend on either electric or chemical actions. The substances that are active in the latter case are called neurotransmitters. A very important member of this family is acetylcholine which is transferred to the cell that receives the signal across the postsynaptic membrane or motor endplate through a... 

Motor end-plate or neuromuscular junction = axon terminal in apposition to specialized surface of muscle cell membrane... 

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... 

At the neuromuscular junction, the terminus of the axon is separated from the sarcolemma by a cleft about 4 nm wide. When an action potential arrives at the terminus, it activates a voltage-sensitive Ca " ion channel. This results in Ca + ions diffusing into the terminus increasing the intracellular Ca + ion concentration, which stimulates exo-cytosis of acetylcholine from the terminus into the cleft. The acetylcholine diffuses across the cleft and binds to receptors on the motor end-plate (Figure 13.12) on the muscle side of the cleft. The binding of acetylcholine to... 

Myasthenia gravis is an autoimmune disease in which antibodies are present in blood and bind to the acetylcholine receptor on the motor end-plate. This prevents the muscles from contracting so that, due to lack of use, they become weak and fatigue easily. In particular, there is difficulty in speaking, swallowing and chewing food. 

Figure 13.12 motor end-plate. The axon terminates very close to the muscle. They are separated by a small gap (the synaptic cleft). When the nerve is stimulated, acetylcholine is released into the cleft where it diffuses across the cleft, and then binds to receptors located on the muscle side of the cleft and initiates an action potential along the sarcolemma. 

Acetylcholine (ACh) as a transmitter. ACh serves as mediator at terminals of all postganglionic parasympathetic fibers, in addition to fulfilling its transmitter role at ganglionic synapses within both the sympathetic and parasympathetic divisions and the motor end-plates on striated muscle. However, different types of receptors are present at these synaptic junctions ... 

Mecfianism of Action A cinchona alkaloid that relaxes skeletal muscle by increasing the refractory period, decreasing excitability of motor end plates (curare-like), and affecting distribution of calcium with muscle fiber. Antimalaria Depresses oxygen uptake, carbohydrate metabolism, elevates pH in intracellular organelles of parasites. Therapeutic Effect Relaxes skeletal muscle produces parasite death. Pharmacokinetics Rapidly absorbed mainly from upper small intestine. Protein binding 70%-95%. Metabolized in liver. Excreted in feces, saliva, and urine. Half-life 8-14 hr (adults), 6-12 hr (children). 

At the neuromuscular junction, it produces the contraction of skeletal muscle by its direct action and by inactivation of anticholinesterase and has got anticurare action. By virtue of its structural similarity to acetylcholine, it acts as partial agonist on motor end plate. 

Myasthenia gravis is an autoimmune disease resulting from production of autoantibodies against AChR at the motor end plate, causing defects in neuromuscular transmission. Depending on the muscles affected a patient may develop dysphagia or respiratory failure [1]. The appearance of pathological forms of erythrocytes such as stomatocytes, echinocytes etc., in peripheral blood causes microcirculation disorders [2]. 

Skeletal muscle relaxation and paralysis can occur from interruption of function at several sites along the pathway from the central nervous system (CNS) to myelinated somatic nerves, unmyelinated motor nerve terminals, nicotinic acetylcholine receptors, the motor end plate, the muscle membrane, and the intracellular muscular contractile apparatus itself. 

As indicated earlier, the relaxant effects of the toxin are likewise temporary, and these effects typically diminish within 2 to 3 months after injection.91 The effects apparently wear off because a new presynaptic terminal sprouts from the axon that contains the originally affected presynaptic terminal. This new terminal grows downward, reattaching to the skeletal muscle and creating a new motor end plate with a new source of acetylcholine. The effects of the previous injection are overcome when this new presynaptic terminal begins to function. Another injection will be needed to block the release from this new presynaptic terminal, thus allowing another 2 to 3 months of antispasticity effects. This fact raises the question of how... 

Motor end plate in skeletal muscle ACh Nicotine d-Tubocurarine ... 

Neuromuscular transmission (B) of motor nerve impulses to the striated muscle fiber takes place at the motor end plate. The nerve impulse liberates acetylcholine (ACh) from the axon terminal. ACh binds to nicotinic cholinoceptors at the motor end plate. This causes depolarization of the postsynaptic membrane, which in turn elicits a propagated action potential (AP) in the surrounding sarcolemma. The AP triggers a release of Ca2+ from its storage organelles, the sarcoplasmic reticulum (SR), within the muscle fiber the rise in Ca2+ concentration induces a contraction (electromechanical coupling). Meanwhile, ACh is hydrolyzed by acetylcholinesterase (p. 104) excitation of the end plate subsides. If no AP follows, Ca2+ is taken up again by the SR and the myofilaments relax. 

The neuromuscular junction is the synapse (junction) of an axon terminal of a motorneuron, which terminates in a depression of the sarcolemma (the cell membrane of a muscle cell), the motor end plate. It is here that the initiation of action potentials across the muscle surface ultimately leads to muscle contraction. In vertebrates, the neurotransmitter is acetylcholine. 

Neuromuscular disease is a very broad term that encompasses many diseases and ailments which either directly, via intrinsic muscle pathology, or indirectly, via nerve pathology, impair the functioning of the muscles. Diseases of the motor end plate include myasthenia gravis and its related condition Lambert-Eaton myasthenic syndrome. Tetanus and botulism are bacterial infections in which bacterial toxins cause increased or decreased muscle tone, respectively. 

There is AChE-like activity in the plasma of some birds and mammals (Traina and Serpietri 1984 Smucker and Wilson 1990). Plasma ChE of rodents, such as the laboratory rat, is high in both AChE and BuChE activities (Traina and Serpietri 1984). AChE activity in human blood is found mainly in RBCs (Silver 1974). AChE activity also occurs in the serum of developing mammals and birds, decreasing to adult levels after birth (Smucker and Wilson 1990). Together with AChEs, BuChEs are also found at synapses, motor end plates, and muscle fibers. BuChE activity in blood is restricted to serum (Silver 1974)... 

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