Physiology of the Neuromuscular Junction
- Introduction. The neuromuscular junction is made up of a motor neurone and a motor endplate with a synaptic cleft or junctional gap dividing them.
- Questions. What is the structure of the neuromuscular junction? ...
- The Motor Neurone. ...
- The Motor Endplate. ...
- Acetylcholine synthesis, storage and release. ...
- Acetylcholine Receptors. ...
- Acetylcholinesterase. ...
- Summary. ...
What are the three components of the neuromuscular junction?
The anatomy of a neuromuscular junction can be divided into three parts:
- the presynaptic terminal (i.e. the motor neuron)
- the synaptic cleft
- the postsynaptic membrane (i.e. the membrane of the muscle cell ).
How do I describe a neuromuscular junction?
The structure of NMJ is divided into three parts:
- Nerve Terminal - The membrane of the nerve terminal has some zones of membrane thickening, and they are known as active zones. ...
- Synaptic Cleft or Junctional Cleft - This is called the space between the plasma membrane and nerve terminal. ...
- Motor End Plate - The motor end plate forms the postsynaptic portion of NMJ. ...
What type of muscle tissue has neuromuscular junctions?
What type of muscle tissue has neuromuscular junctions? skeletal muscle. surrounded by perimysium. fasciculus. Endomysium is a delicate network of loose connective tissue that. ... neuromuscular junctions. Synaptic vesicles in the neuromuscular junction contain. acetylcholine.
What occurs in the neuromuscular junction?
- Components.
- The synaptic end bulb.
- The motor end plate.
- The synaptic cleft.
- Clinical significance. Botulinum toxin. Curare. Anticholinesterase agents.
- Skeletal muscle tissue. Neurons: Structure and types.
What is the function of a neuromuscular junction?
The neuromuscular junction (NMJ) is a highly specialized synapse between a motor neuron nerve terminal and its muscle fiber that are responsible for converting electrical impulses generated by the motor neuron into electrical activity in the muscle fibers.
What are the steps of neuromuscular junction?
Terms in this set (7)1) An AP travels down the axon. to the axon terminal.2) Electrical gated calcium channels open. ... 3) Calcium causes the vesicles to. ... 4) ACH diffuses across the synaptic cleft. ... 5) ACH binding opens ion channels. ... 6) If the muscle reaches the threshold (-55mv) at the motor end plate. ... 7) ACH is broken down by.
What are characteristics of a neuromuscular junction?
The NMJs of all vertebrates display the same basic features: (1) an axon terminal containing the neurotransmitter, ACh, in many small, clear vesicles; (2) an overlying Schwann cell (teloglia) that covers the axon terminal except at the interface of the presynaptic and postsynaptic membranes; (3) an area of synaptic ...
What is the physiology of muscle contraction?
The physiological concept of muscle contraction is based on two variables: length and tension. In physiology, muscle shortening and muscle contraction are not synonymous, as tension within the muscle can be produced without changes in the length of the muscle.
What is neuromuscular physiology?
The neuromuscular junction (NMJ) is a synaptic connection between the terminal end of a motor nerve and a muscle (skeletal/ smooth/ cardiac). It is the site for the transmission of action potential from nerve to the muscle. It is also a site for many diseases and a site of action for many pharmacological drugs.
What is nerve muscle physiology?
NERVE + MUSCLE+PHYSIOLOGY. Nerve: The filamentous bands of nervous tissue that connect. parts of the nervous system with the other organs, conduct nerve impulses and are made up of axons and.
Which event occurs at the neuromuscular junction?
At the neuromuscular junction, the nerve fiber is able to transmit a signal to the muscle fiber by releasing ACh (and other substances), causing muscle contraction.
What is the function of the neuromuscular junction quizlet?
What is the function of the Neuromuscular Junction? Transmit motor neuron to the skeletal muscle fibre quickly and reliably, to ensure precise control of skeletal muscle contraction and therefore voluntary movement.
What does a neuromuscular junction contain?
The neuromuscular junction contains the terminal nerve branch with its specialized presynaptic ending, which lies in a specialized trough of the postsynaptic muscle plasma membrane (sarcolemma). A synaptic cleft separates the two membranes.
What physiological events happen in each part of the simple muscle twitch?
A single muscle twitch has three components. The latent period, or lag phase, the contraction phase, and the relaxation phase. The latent period is a short delay (1-2 msec) from the time when the action potential reaches the muscle until tension can be observed in the muscle.
What is a muscle twitch physiology?
Muscle twitching is caused by minor muscle contractions in the area, or uncontrollable twitching of a muscle group that is served by a single motor nerve fiber. Muscle twitches are minor and often go unnoticed. Some are common and normal. Others are signs of a nervous system disorder.
What is the order of physiological events that leads to a muscle movement?
Terms in this set (7) ACh binds receptors on the motor end plate, initiating a muscle impulse. Calcium ions bind to troponin, causing tropomyosin to move and expose active sites. Myosin heads attach to actin and form crossbridges. A cyclic "attach, pivot, detach, return" event occurs.
What are the 3 main phases of the neuromuscular action potential?
An action potential has three phases: depolarization, overshoot, repolarization.
What are the 4 basic steps in the sliding filament theory?
In the sliding filament theory, myosin heads attach to an actin filament, bend to pull the actin filaments closer together, then release, reattach, and pull again.
What are the 4 basic steps in the sliding filament theory *?
Phosphate release by myosin triggers the actual power contraction stroke.ADP pocket opens up on the myosin head.Myosin head rotates and releases the ADP.As the head rotates it moves in a ratchet like motion and pulls the thin filaments closer to the center of the M line of the sarcomere.
What are the steps that take place at a neuromuscular junction that lead to muscle contraction?
When the nervous system signal reaches the neuromuscular junction a chemical message is released by the motor neuron. The chemical message, a neurotransmitter called acetylcholine, binds to receptors on the outside of the muscle fiber. That starts a chemical reaction within the muscle.
Why is the neuromuscular junction important?
The neuromuscular junction is so vital to life that everything is done to excess, excess transmitter release, excess receptor numbers and an excessive post-synaptic potential to ensure transmission of the stimulus and skeletal muscle contraction. Tutorial Outline.
How many neuromuscular junctions are there in each muscle?
There is however only one neuromuscular junction on each skeletal muscle fibre, any others are eliminated during development. As the motor neurone enters a muscle, the axon divides into telodendria, the ends of which, the terminal buttons, synapse with the motor endplate. The two are separated by approximately 20nm, ...
Where are the extra junctional receptors located?
The extra-junctional receptors can be present anywhere on the muscle membrane usually in extremely small numbers, though they are found in their greatest concentration around the endplate in the peri-junctional zone. Denervation injuries and burns are associated with large increases in the number of extra-junctional receptors on the muscle membrane. The extra- junctional receptors have the structure of immature foetal receptors (ε subunit replaced by a γ subunit). This affects the physiology and pharmacology of the receptor with increased sensitivity to depolarising muscle relaxants and reduced sensitivity to non-depolarising muscle relaxants.
How many vesicles are readily releasable?
The vesicles then become part of one of three pools or stores, each varying in their availability ability for release. About 1% are immediately releasable, about 80% are readily releasable and the remainder form the stationary store. The exact proportions may vary depending on the level of demand or nerve stimulation.
Which receptors have the structure of immature foetal receptors?
The extra- junctional receptors have the structure of immature foetal receptors (ε subunit replaced by a γ subunit). This affects the physiology and pharmacology of the receptor with increased sensitivity to depolarising muscle relaxants and reduced sensitivity to non-depolarising muscle relaxants.
What is the area of muscle around the motor endplate?
The clefts of the motor endplate contain acetylcholinesterase. The area of muscle around the motor endplate is the peri-junctional zone. It is here that the potential developed at the endplate is converted to an action potential that propagates through the muscle to initiate contraction.
What is the cell body of a neuron?
The cell body of a neurone is at its proximal end and information travels from here down the axon. Axons are 10-20μm in diameter and surrounded by a myelin sheath produced by Schwann cells. This acts as an insulator to speed up nerve conduction.
What is the neuromuscular junction?
Neuromuscular junction (NMJ) is responsible for the chemical transmission of the electrical impulse from a nerve to the muscle( skeletal/ smooth/ cardiac) in order to produce an appropriate muscle contraction. Diseases of NMJ such as myasthenia gravis, Lambert-Eaton syndrome, and botulism affects neuromuscular impulse transmission and result in muscle weakness and paralysis. Many drugs and anesthetic agents also affect neuromuscular junction and impulse transmission to elicit their effects. In order to understand the pathophysiology and basis of treatment of the diseases that affect neuromuscular transmission, it is important to have a thorough knowledge of the structure of NMJ and the physiology of neuromuscular transmission.[1][2][3]
What is the neuromuscular junction of smooth muscle?
The neuromuscular junction of the smooth muscle is not as highly structured as skeletal muscle NMJ. Smooth muscle NMJ is formed between the autonomic nerve fibers that branch diffusely on smooth muscle to form diffuse junctions. The autonomic nerve in smooth muscle NMJ does not have typical nerve terminals as seen in skeletal NMJ, but instead, it has multiple varicosities distributed along its axis. Unlike skeletal NMJ that always has Ach as a neurotransmitter, the SVs present in the varicosities may contain ACh or norepinephrine, or another transmitter. The Schwann cells are interrupted at the points where varicosities are present so that neurotransmitters can diffuse to the cells. The smooth muscles have many layers of muscle cells, but the nerve fibers often innervate only the outer layer. Muscle excitation travels from this outer layer to the inner layers by action potential conduction in the muscle mass or additional diffusion of the transmitter substance. In body parts where smooth muscle activity is relatively slow, like intestines, one neuron controls a large number of muscle fibers, but parts where the activity is fast, such as iris, the autonomic nerve branch less extensively and controls fewer muscle fibers. [2][3]
What drugs can cause skeletal muscle paralysis?
Drugs like succinylcholine also paralyze the skeletal muscle but through continued depolarization that prevents repolarization of the motor endplate, resulting in ACh receptors becoming desensitized and inactivated. These drugs are used in general anesthesia to help avoid large doses of general anesthetics. Administration of neuromuscular blocking agents and drugs can also result in bulbar and respiratory muscle failure. ACh esterase inhibitors like physostigmine neostigmine, pyridostigmine, and edrophonium increase the levels of ACh in the synaptic cleft. Physostigmine and neostigmine are used for the treatment of Myasthenia Gravis (MG). Irreversible inhibitors of ACh esterase include the organophosphates commonly used as an insecticide, which include malathion and parathion. Exposure to these may cause organophosphate toxicity syndrome that includes diarrhea, urination, myosis, bronchospasm, excessive lacrimation, and salivation. The effects of irreversible inhibitors of ACh esterase can be reversed by using a competitive inhibitor such as atropine and/or pralidoxime, which regenerates ACh esterase if given early enough before enzyme aging occurs. [7][12]
What is the most common neuromuscular junction disease?
Among the most common diseases of the skeletal neuromuscular junction is myasthenia gravis (MG). In over 60% of cases, hyperplasia of the thymus gland is present when excessive T cells may predispose to an autoimmune response. MG is an autoimmune disorder in which the body produces antibodies against its own ACh receptors in the postsynaptic membrane. These antibodies bind to the ACh receptors and block the interaction of ACh with them, resulting in the blockage of NMJ transmission, muscle weakness, and paralysis. Acetylcholine receptor antibodies are present in about 85% of patients with generalized symptoms, but only 50% of patients with purely ocular involvement MG characteristically presents with double vision (diplopia), drooping of the upper eyelids (ptosis), difficulty in speaking (dysarthria), difficulty in swallowing (dysphagia) and general muscle fatigue. The symptoms are typically least expressed in the morning and are worse in the evening as the amount of ACh bound to the postsynaptic membrane receptor decreases due to various muscle activities during the day. In the progressive form of the disease, the weakness may become steadily worse, may cause myasthenic crisis and death. Decrement of over 10% observed following repetitive nerve stimulation is a diagnostic criterion for MG due to depletion of functional ACh in the synaptic cleft. [6][4]
How does calcium affect the action potential?
When the nerve impulse from the peripheral or central nervous system reaches the presynaptic membrane (nerve terminal) of the neuromuscular junction in the form of the action potential, it triggers voltage-gated Ca2+ channels at the active zones of the nerve terminal to open, and Ca2+ ions enter the nerve terminal from the extracellular space. Increased intracellular calcium interact with SNARE proteins; this stimulates synaptic vesicles to fuse with active zones and release their content – ACh into the synaptic cleft. This process is named exocytosis. Increased intracellular calcium in nerve terminals triggers the simultaneous release of a number of ACh quanta. The total number of quanta of ACh released by a stimulated nerve markedly depends on the concentration of Ca2+ ions in the extracellular fluid. If Ca2+ ions are not present, even electrical stimulation of the nerve will not produce the release of transmitter. A 2-fold increase in the extracellular calcium will cause a 16-fold increase in the quantal content of an endplate potential.
What causes a skeletal muscle to be weak?
LEMS is another autoimmune disease affecting skeletal muscle NMJ when the body produces antibodies against its own presynaptic membrane Ca2+ channels. Blocking Ca2+ channels in the presynaptic membrane leads to less calcium entry into the nerve terminal and less ACh being released, resulting in weakness of skeletal muscles and fatigue that usually improves after physical activity. The exact cause of LEMS is unknown but correlates with tumors of the lung, usually small cell lung cancer. The symptoms of LES are similar to MG, such as muscle weakness and fatigue; however, what separates LES from MG is that in LES, proximal limb muscles are involved in the presence of depressed tendon reflexes a weakness improves with use. This is because with repeated attempts at muscle contraction, a calcium gradient builds up outside the presynaptic Ca channel, eventually allowing the endogenous calcium to outcompete the auto-antibodies to trigger the release of ACh in the synaptic cleft. 80% of LES patients complain of proximal muscle weakness in both arms and legs. Oropharyngeal and ocular muscles are mildly affected so, eyelid ptosis and mild diplopia may also be present. Autonomic symptoms such as dry mouth, constipation, impotence in males, and postural hypotension may be seen. The triad of proximal muscle weakness, areflexia, and autonomic dysfunction aids in making the diagnosis. The increased response following repetitive nerve stimulation is a diagnostic criterion for LEMS due to increased Ca2+ after supra-maximal stimulation, resulting in increased functional ACh in the synaptic cleft. [4]
What is neuromuscular transmission failure?
These disease states produce weakness of muscles of eyes, face, limbs, respiration, etc. Though the clinical presentation of these diseases may appear similar, there are important differences in the etiology and the basis of treatment. [4].
What is the function of the neuromuscular junction?
The neuromuscular junction then, is a key component in the body’s ability to produce and control movement. Amazingly, processes at the neuromuscular junction take place at speeds that allow movements to occur with no appreciable delay or lag. This article will discuss the anatomy and function of the neuromuscular junction.
What is the junction between the brain and the spinal cord?
At its simplest, the neuromuscular junction is a type of synapse where neuronal signals from the brain or spinal cord interact with skeletal muscle fibers, causing them to contract.
What happens when the synaptic vesicles move towards the cell membrane?
The increase of Ca2+ within the cytosol of the synaptic end bulb causes the synaptic vesicles to move towards and fuse with the neuron’s cell membrane. Once fused, the synaptic vesicles exocytose (release) their contents – ACh – into the synaptic cleft. The ACh then moves across the synaptic cleft towards the motor end plate of the muscle fiber.
What is the space between the synaptic end bulbs of the neuron and the cell membrane of the muscle fiber?
Between the synaptic end bulbs of the neuron and the cell membrane of the muscle fiber (the sarcolemma) lies a space known as the synaptic cleft, which is the final component of the neuromuscular junction.
What is the axon terminal?
At this point, each axon of the motor neuron will divide into branches called axon terminals. Towards the end of the axon terminal, closest to the muscle fiber, the tip of the axon terminal enlarges and becomes known as the synaptic end bulb. It is the synaptic end bulb of the motor neuron that comprises the nervous system component ...
What is the chemical that moves the electrical signal across the synaptic cleft?
The chemical in this case is acetylcholine (ACh), an example of a neurotransmitter that allows neurons to communicate with other cells.
Where is the motor end plate located?
There is one neuromuscular junction associated with each muscle fiber, and it is typically located near the middle of the fiber. This means that the motor end plate will also be located ...
Where is the neuromuscular junction located?
The neuromuscular junction, therefore, is only found in lower motoneurons. Even the cranial nerves which innervate the muscles of the skull and face synapse with the cell bodies of lower motor neurons in an area called the motor nucleus. Parts of the motor neuron. The important part of the motoneuron in terms of the NMJ is the terminal end.
What are the parts of the neuromuscular junction?
The neuromuscular junction is composed of three parts: Presynaptic motor nerve terminal. Synaptic cleft or junctional cleft. Postsynaptic muscle fiber. To better understand what a neuromuscular junction is, we should first look at the structure of the motor neuron terminal (1, 3), the synaptic cleft (2), and muscle membrane (4, 5).
What neurotransmitter is released at the neuromuscular junction?
What neurotransmitter is released at the neuromuscular junction? Only one – acetylcholine. Acetylcholine levels are regulated by quantity, the effects of muscarinic AChRs in the presynaptic membrane, and the presence and quantity of acetylcholinesterase in the synaptic cleft.
What is the NMJ?
Definition. The neuromuscular junction (NMJ) is the connecting area between the end of a motor neuron and a muscle. It is here that the acetylcholine-dependent nerve impulse ( action potential) is transmitted from neuron to muscle – hence the term neuromuscular. Sometimes referred to as the motor endplate, the NMJ is composed ...
What is a genetic disorder of the neuromuscular junction?
Myasthenia gravis – a debilitating disease. Genetic forms of neuromuscular junction disorders span diseases such as muscular dystrophy and the group of congenital myasthenic syndromes. In muscular dystrophy, damage to muscle tissue also affects the postsynaptic membrane of the sarcolemma.
What happens to muscles without ACHE?
Without AChE, our muscles would regularly twitch. When acetylcholine is released from the terminal end, receptors on the target tissue accept it and signal that tissue to react. This reaction requires calcium ions (see neuromuscular junction steps).
What is the important part of the motor neuron?
Parts of the motor neuron. The important part of the motoneuron in terms of the NMJ is the terminal end. Where the terminal end begins, the insulating myelin layer that covers the axon is lost. At this point, the nerve branches into one to two hundred nerve terminals.
