Neuromuscular Junction, Animation

(USMLE topics) The neuron-muscle relationship and generation of action potential in skeletal muscle cell.
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Voice by: Ashley Fleming
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A skeletal muscle contracts only when stimulated by nerve impulses from a motor neuron.
The axon of a motor neuron usually gives out many branches, supplying multiple muscle fibers. These fibers constitute a motor unit. Small motor units are found in muscles that require finer control, for example, muscles that are responsible for subtle movements of the eyes. Large motor units are found in larger muscles that require strength, such as muscles of the arms and legs.
The strength of a muscle contraction is determined by the number of motor units that are activated at one time. Even at rest, most muscles are in a partial contraction state, called muscle tonus, which is maintained by alternating activation of a small number of motor units.
The connection between a motor neuron and a muscle fiber is called a neuromuscular junction, which is basically a chemical synapse between the nerve terminal and a specialized area of muscle cell membrane called the motor end-plate. When an action potential reaches the nerve terminal, it causes the release of the neurotransmitter acetylcholine into the synaptic space. Acetylcholine then binds to nicotinic receptors on the end-plate. Nicotinic receptors are ligand-gated ion channels. Upon binding to acetylcholine, they open to allow sodium to enter the cells, depolarizing the cell membrane, producing the so-called end-plate potential.
An action potential is generated in the muscle cell only when the end-plate potential reaches the threshold required to activate voltage-gated sodium channels located outside the end-plate, in the neighboring membrane. When activated, these channels allow faster influx of sodium, further depolarizing and eventually reversing the polarity of the cell membrane. At this point, voltage-gated potassium channels open for potassium to move out, quickly returning membrane voltage to its original resting value.
Once generated, the action potential spreads like a wave thanks to similar voltage-gated ion channels located throughout the muscle fiber. The action potential also runs deep into the fiber via T-tubules, to reach the sarcoplasmic reticulum. Here, it activates voltage-gated calcium channels, releasing calcium from the sarcoplasmic reticulum into the cytosol of muscle cells. Calcium then sets off muscle contraction by the “sliding filament mechanism”. This mechanism is described in another video.
Another important component of the neuromuscular junction is the enzyme acetylcholinesterase. This enzyme removes all acetylcholine molecules that do not immediately bind with a receptor and those that are done activating a receptor. The enzyme action essentially terminates synaptic activation, giving the muscle time to relax, and thus preventing continuous contraction that would result in muscle spasms.
Substances that cause muscle weakness or paralysis do so by interfering with the function of neuromuscular junction:
Botulinum toxin prevents acetylcholine release from the presynaptic side of the junction.
Some other toxins attach to nicotinic receptor, blocking acetylcholine from binding, but do not open the ion channel.
Certain drugs lodge into the channel of nicotinic receptor, blocking the passage of sodium.
All these substances prevent activation of muscle cells and cause flaccid paralysis.
On the other hand, some pesticides inhibit acetylcholinesterase, preventing degradation of acetylcholine, causing continuous activation of muscles. That’s how they induce muscle spasms and cause spastic paralysis.

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Otot rangka berkontraksi hanya jika dirangsang oleh impuls saraf dari neuron motorik.
Akson dari neuron motorik biasanya menghasilkan banyak cabang, memasok banyak serat otot. Serat ini merupakan unit motorik. Unit motorik kecil ditemukan di otot yang memerlukan kontrol lebih baik, misalnya otot yang bertanggung jawab atas gerakan halus mata. Unit motorik besar terdapat pada otot yang lebih besar yang membutuhkan kekuatan, seperti otot lengan dan kaki.
Kekuatan kontraksi otot ditentukan oleh banyaknya unit motorik yang diaktifkan pada satu waktu. Bahkan saat istirahat, sebagian besar otot berada dalam keadaan kontraksi parsial, yang disebut tonus otot, yang dipertahankan dengan aktivasi sejumlah kecil unit motorik secara bergantian.
Hubungan antara neuron motorik dan serat otot disebut sambungan neuromuskuler, yang pada dasarnya adalah sinapsis kimiawi antara terminal saraf dan area khusus membran sel otot yang disebut pelat ujung motorik. Ketika potensial aksi mencapai terminal saraf, itu menyebabkan pelepasan neurotransmitter asetilkolin ke ruang sinaptik. Asetilkolin kemudian mengikat reseptor nikotinik pada pelat ujung. Reseptor nikotinik adalah saluran ion berpagar ligan. Setelah mengikat asetilkolin, mereka terbuka untuk memungkinkan natrium memasuki sel, mendepolarisasi membran sel, menghasilkan apa yang disebut potensi pelat-ujung.
Potensial aksi dihasilkan dalam sel otot hanya ketika potensial pelat-ujung mencapai ambang yang diperlukan untuk mengaktifkan saluran natrium berpagar tegangan yang terletak di luar pelat-ujung, di membran tetangga. Ketika diaktifkan, saluran ini memungkinkan masuknya natrium lebih cepat, depolarisasi lebih lanjut dan akhirnya membalikkan polaritas membran sel. Pada titik ini, saluran kalium dengan gerbang tegangan terbuka untuk memindahkan kalium keluar, dengan cepat mengembalikan tegangan membran ke nilai istirahat aslinya.
Setelah dihasilkan, potensial aksi menyebar seperti gelombang berkat saluran ion berpagar tegangan serupa yang terletak di seluruh serat otot. Potensi aksi juga mengalir jauh ke dalam serat melalui tubulus-T, untuk mencapai retikulum sarkoplasma. Di sini, ia mengaktifkan saluran kalsium dengan gerbang tegangan, melepaskan kalsium dari retikulum sarkoplasma ke dalam sitosol sel otot. Kalsium kemudian memicu kontraksi otot dengan "mekanisme filamen geser". Mekanisme ini dijelaskan di video lain.
Komponen penting lain dari sambungan neuromuskuler adalah enzim asetilkolinesterase. Enzim ini menghilangkan semua molekul asetilkolin yang tidak segera mengikat dengan reseptor dan yang dilakukan mengaktifkan reseptor. Tindakan enzim pada dasarnya menghentikan aktivasi sinaptik, memberi waktu otot untuk rileks, dan dengan demikian mencegah kontraksi terus menerus yang akan mengakibatkan kejang otot.
Zat yang menyebabkan kelemahan otot atau kelumpuhan melakukannya dengan mengganggu fungsi sambungan neuromuskuler:
- Toksin botulinum mencegah pelepasan asetilkolin dari sisi sambungan presinaptik.
- Beberapa racun lain menempel pada reseptor nikotinik, menghalangi pengikatan asetilkolin, tetapi tidak membuka saluran ion.
- Obat-obatan tertentu masuk ke saluran reseptor nikotinik, menghalangi jalannya natrium.
Semua zat ini mencegah aktivasi sel otot dan menyebabkan kelumpuhan lembek.
Di sisi lain, beberapa pestisida menghambat asetilkolinesterase, mencegah degradasi asetilkolin, menyebabkan aktivasi otot secara terus menerus. Begitulah cara mereka menyebabkan kejang otot dan menyebabkan kelumpuhan kejang.

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There seems to be a mistake during 2:36, when talking about bringing the voltage back to its resting potential, truth is, no hyperpolarization should occur. The voltage doesnt go below -95V.
Otherwise great vid Alila, hopefully people didnt fail based on that mishap.

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why was number three blurred when it was describing the Neuromuscular Toxins? 4:26

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1:31 neuromuscular junction

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Where the potassium ions located

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When there is action potential there is muscle contraction

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What was the 3rd toxin

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What is #3 at 4:10?

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What is mean by cytoplasmic

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1:30