★ISPN/RN Review ★ The Neuromuscular Junction 神经肌肉接头
Nerves communicate with muscles at a synapse called the neuromuscular junction (NMJ). At this point, a nerve stimulates a muscle to contract. If the nerve is not able to communicate with the muscle cell, the muscle will not be able to contract, and paralysis will result. Certain clinical situations require that a patient not be able to move muscles, including surgery, diagnostic procedures, and mechanical ventilation. Anesthetics can prevent muscle movement by suppressing function through the central nervous system (CNS), with many systemic complications from this depression. The NMJ blocking drugs are used to prevent the nerve stimulation at the muscle cell and cause paralysis of the muscle directly without total CNS depression and its many systemic effects.
The neuromuscular junction is the point at which a motor neuron communicates with a skeletal muscle fiber. The end result is muscular contraction. NMJ blocking agents affect the normal functioning of muscles by interfering with the normal processes that occur at the junction of nerve and muscle cell.
The functional unit of a muscle, called a sarcomere, is made up of light and dark filaments formed by actin and myosin molecules. These molecules are arranged in orderly stacks that give the sarcomere a striated or striped appearance. Normal muscle function involves the arrival of a nerve impulse at the motor nerve terminal, followed by the release of the neurotransmitter acetylcholine (ACh) into the synaptic cleft. At the acetylcholine receptor site on the effector side of the synapse, the ACh interacts with the nicotinic cholinergic receptors, causing depolarization of the muscle membrane. ACh is then broken down by acetylcholinesterase (an enzyme), freeing the receptor for further stimulation. With stimulation, this depolarization allows the release of calcium ions, stored in tubules, into the cell. The calcium binds to troponin, a chemical found throughout the sarcomere. This binding of troponin releases the actin- and myosin-binding sites, allowing them to react with each other. The actin and myosin molecules react with each other again and again, sliding along the filament and making it shorter. This is a contraction of the muscle fiber according to the sliding filament theory. As the calcium is removed from the cell during repolarization of the muscle membrane the troponin is freed and once again prevents the actin and myosin from reacting with each other. The muscle filament then relaxes or slides back to the resting position.
A dynamic balance of excitatory and inhibitory impulses to the muscle results in muscle tone. However, if ACh cannot react with the cholinergic muscle receptor or if the muscle cells cannot repolarize to allow new stimulation and muscle contraction, muscle paralysis, or loss of muscle function, occurs.
synapse – n. 突触
junction – n. 接点,接头,联结
neuromuscular junction (NMJ) – 神经肌肉接头
paralysis – n. 麻痹,瘫痪
motor neuron – 运动神经元
sarcomere – n. 肌节
filament – n. (肌)丝,带
actin – n. 肌动蛋白
myosin – n. 肌球蛋白
stack – n. 堆,栈,束
striated – a. 有条纹的,纹状的
striped – a. 有斑纹的
nerve terminal – 神经末梢
acetylcholine (ACh) – n. 乙酰胆碱
synaptic cleft – 突触间隙
effector – n. 效应器,受动器
nicotinic – a. 烟碱的
cholinergic – a. 胆碱能的
depolarization – n. 去极化,除极
acetylcholinesterase – 乙酰胆碱酯酶
tubule – n. (肌)管
troponin – n. 肌钙蛋白
sliding filament – 肌丝滑行
repolarization – n. 再极化,复极
repolarize – v. 再极化
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★Video★
Neuromuscular Junction
★Test ★
1. Repeated stimulation of cholinergic receptors is possible because:
A. The receptor is liberated
B. Nerve impulses arrive at the motor nerve terminal
C. ACh interacts with the nicotinic cholinergic receptors
D. The troponin is freed 2. NMJ blockers are used in surgery, diagnostic procedures, and mechanical ventilation because:
A. They cause many systemic complication by suppressing function through CNS
B. They cause nerve stimulation at the muscle cell by sending nerve impulse
C. They prevent nerve stimulation by interfering with the arrival of nerve impulse at the motor nerve terminal
D. They cause paralysis of the muscle with systemic effects
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答案 Answers 1. A. The receptor is liberated Rationale: At the acetylcholine receptor site on the effector side of the synapse, the ACh interacts with the nicotinic cholinergic receptors, causing depolarization of the muscle membrane. ACh is then broken down by acetylcholinesterase, freeing the receptor for further stimulation. 2. C. They prevent nerve stimulation by interfering with the arrival of nerve impulse at the motor nerve terminal Rationale: The NMJ blockers are used to prevent nerve stimulation at the muscle cell and casue paralysis of the muscle directly without total CNS depression and its many systemic effects. They affect the normal functioning of muscles by interfering with the normal processes that occur at the junction of nerve and muscle cell, including the arrival of a nerve impulse at the motor nerve terminal.