Name: calcium control in muscle contraction
Uploaded: 2025-10-23T11:47:01.000Z
Duration: 1 min 26 s
Channel: JoVE

K12 Standards

Florida Department of Education

High School

Life Science

SC.912.L.14

SC.912.L.14.17

Cross-bridge Cycle

تنقبض العضلات عندما يزيد تداخل الشعيرات الرقيقة والسميكة مما يؤدي إلى انخفاض طول القسيم على المستوى الجزيئي يحدث الانكماش عندما يتم تحلل ATP المرتبط بمنطقة الرأس الكروي للميوسين إلى ADP،مما يحول رأس الميوسين إلى حالة طاقة عالية يرتبط فيها بالأكتين ويخلق جسرًا متقاطعاًيؤدي إطلاق ADP إلى عودة رأس الميوسين إلى حالة الطاقة المنخفضة،مما يؤدي إلى تحريك الأكتين باتجاه مركز القطعة العضلية ربط جزيء ATP جديد برأس الميوسين ثم فصله عن الأكتين في المرة التالية التي يكون رأس الميوسين مرتبطاًبالأكتين سيكون على جزء أقرب إلى الخط Z يتم التحكم في عملية الربط هذه بواسطة بروتينين تنظيميين التروبوموسين والتروبونين وتركيز الكالسيوم الذي يتم تخزينه وإطلاقه من شبكية الساركوبلازم يغطي التروبوموسين موقع ربط الميوسين على الأكتين ويرتبط التروبونين بالكالسيوم عندما يكون ذلك متاحاًمع نقل التروبوميوسين بعيداًعن موقع ربط الميوسين على الأكتين في هذا التأكيد يمكن أن يتشكل جسر متقاطع وتنكمش العضلات تستمر هذه الدورة حتى لم يعد الكالسيوم و ATP موجودين في ألياف العضلات

جوليش ، عزيز ، إليسا نيجروني ، فاليري ديكوستر ، ألكسندر ديمول ، وكاثرين كويرولت. "خصائص الجسور المتقاطعة المتغيرة في ضمور العضلات الهيكلية". الحدود في علم وظائف الأعضاء 5 (14 أكتوبر 2014). [<a href = "https://doi.org/10.3389/fphys.2014.00393" target = "__blank" >المصدر</a>]

ديبولد ، إدوارد ب. "رؤى حديثة حول إجهاد العضلات على مستوى الجسر المتقاطع". الحدود في علم وظائف الأعضاء 3 (1 يونيو 2012). [<a href = "https://doi.org/10.3389/fphys.2012.00151" target = "__blank" >مصدر</a>]

رال ، جاك أ. "ما الذي يجعل العضلات الهيكلية مخططة؟ اكتشافات في الهيكل الخلوي للذميات الداخلية والهيكل الخلوي الخارجي ". التقدم في تعليم علم وظائف الأعضاء 42 ، العدد 4 (15 نوفمبر 2018): 672-84. [<a href = "https://doi.org/10.1152/advan.00152.2018" target = "__blank" >المصدر</a>]

دورة عبور الجسر

مع انقباض العضلات ، يزداد التداخل بين الخيوط الرفيعة والسميكة ، مما يقلل من طول القسيم العضلي _ الوحدة الانقباضية للعضلة _ استخدام الطاقة في شكل أدينوسين ثلاثي الفوسفات. على المستوى الجزيئي ، هذه عملية دورية متعددة الخطوات تتضمن الارتباط والتحلل المائي لأدينوسين ثلاثي الفوسفات ، وحركة الأكتين بواسطة الميوسين.

عندما يتحلل جزيء أدينوسين ثلاثي الفوسفات ، المرتبط برأس الميوسين ، إلى أدينوسين ثنائي الفوسفات ، ينتقل الميوسين إلى حالة طاقة عالية مرتبطة بالأكتين ، مما يؤدي إلى تكوين جسر متقاطع. عندما يتم تحرير الأدينوسين ثنائي الفوسفات ، يتحرك رأس الميوسين إلى حالة طاقة منخفضة ، محركاً الأكتين نحو مركز القسيم العضلي. يؤدي ارتباط جزيء أدينوسين ثلاثي الفوسفات الجديد إلى فصل الميوسين عن الأكتين. عندما يتم تحلل أدينوسين ثلاثي الفوسفات هذا ، سيرتبط رأس الميوسين بالأكتين ، هذه المرة على جزء من الأكتين أقرب إلى نهاية القسيم العضلي. تعمل البروتينات التنظيمية تروبونين وتروبوميوسين ، جنباً إلى جنب مع الكالسيوم ، معاً للتحكم في تفاعل الميوسين-أكتين. عندما يرتبط التروبونين بالكالسيوم ، يتم نقل التروبوميوسين بعيداً عن موقع ارتباط الميوسين على الأكتين ، مما يسمح للميوسين والأكتين بالتفاعل ويحدث تقلص العضلات.

<h4>الكالسيوم</h4>

كمنظم لتقلص العضلات ، يتم التحكم في تركيز الكالسيوم عن كثب في ألياف العضلات. ألياف العضلات على اتصال وثيق مع الخلايا العصبية الحركية. تتسبب إمكانات العمل في الخلايا العصبية الحركية في إطلاق الناقل العصبي أستيل كولين بالقرب من ألياف العضلات. ينتج عن هذا جهد فعل (إزالة الاستقطاب) في الخلية العضلية ، يتم حمله على طول غشاء البلازما ومن خلال غشاء البلازما التي تسمى المستعرضة أو الأنابيب التائية.

<تتوغل الأنابيب التائية في عمق العضلات وتكون مجاورة لعضيات شبكية إندوبلازمية متخصصة تسمى الشبكة الساركوبلازمية أو SR. يتم تحرير الكالسيوم المحتجز داخل الشبكة الساركوبلازمية عندما تنفتح القنوات الأيونية ذات الجهد الكهربائي (القنوات الأيونية التي تفتح وتغلق بناءً على الشحنات المحلية) استجابةً لإزالة الاستقطاب ، مما يسمح لأيونات الكالسيوم بالدخول إلى السيتوبلازم ، وتقلص العضلات.

عندما تتوقف الإشارات من الخلايا العصبية الحركية ، يبدأ استرخاء العضلات حيث يتم ضخ الكالسيوم مرة أخرى في الشبكة الساركوبلازمية ، مما يقلل من مستويات الكالسيوم في السيتوبلازم ويجدد مخازن الكالسيوم الشبكة الساركوبلازمية استعداداً للانكماش التالي.

<h4>تنكس العضلات</h4>

يمكن أن تنقبض العضلات السليمة ولكن العضلات المريضة تفقد هذه القدرة غالباً. تمنع أمراض مثل الوهن العضلي الوبيل تحفيز الخلايا العصبية الحركية للعضلات مما يؤدي إلى ضمور العضلات وانخفاض كتلة العضلات. يتسبب التصلب الجانبي الضموري (ALS أو مرض لو جيهرنج) في تدهور الخلايا العصبية الحركية ، مما يؤدي بالمثل إلى تنكس العضلات وضمورها.

مع تقلص العضلات ، يزداد التداخل بين الخيوط الرفيعة والسميكة ، مما يقلل من طول القشر العضلي - الوحدة الانقباضية ل ...

Education

JoVE Core

Biology

علم الأحياء

Human Biology

بيولوجيا الإنسان

Musculoskeletal System

الجهاز العضلي الهيكلي

KEY TERMS AND CONCEPTS

المصطلحات والمفاهيم الأساسية

calcium control in muscle contraction

Calcium control in muscle contraction depends on ATP, motor neurons, and the sliding action of actin and myosin. As a muscle contracts, the thin and thick filaments overlap more, and the sarcomere, which is the contractile unit of the muscle, becomes shorter. This process uses energy from ATP and happens in a repeating cycle at the molecular level.

Myosin drives the movement of actin through a cross-bridge cycle. When ATP attached to the myosin head is hydrolyzed to ADP, myosin shifts into a high-energy state and binds actin. This forms a cross-bridge. When ADP is released, the myosin head moves to a lower-energy state and pulls actin toward the center of the sarcomere. A new ATP molecule then binds to myosin and causes it to detach from actin. After that ATP is hydrolyzed, myosin can bind again, this time to a new site on actin closer to the end of the sarcomere.

Troponin, tropomyosin, and calcium regulate this interaction. When troponin binds calcium, tropomyosin moves away from the myosin-binding site on actin. That shift lets myosin and actin interact, and muscle contraction can occur. Calcium concentration in muscle fibers is tightly controlled so this switch can happen at the right time.

Motor neurons start the process by signaling nearby muscle fibers. Their action potentials trigger release of the neurotransmitter acetylcholine near the muscle cell. This produces an action potential, or depolarization, in the muscle cell membrane. The signal travels along the plasma membrane and through T-tubules, which are inward folds of the membrane that carry the signal deep into the muscle. T-tubules sit next to the sarcoplasmic reticulum, or SR, a specialized endoplasmic reticulum that stores calcium.

When depolarization reaches the SR, voltage-gated ion channels open and release calcium into the cytoplasm. The rise in calcium allows the muscle to contract. When signaling from the motor neuron stops, relaxation begins. Calcium is pumped back into the SR, which lowers calcium in the cytoplasm and restores the SR calcium supply for the next contraction.

Healthy muscle can contract, but diseased muscle may lose that ability. Myasthenia gravis can prevent motor neuron stimulation of muscle, which can lead to muscle atrophy and a decrease in muscle mass. Amyotrophic lateral sclerosis, or ALS, also called Lou Gehrig's disease, causes motor neurons to degenerate. That loss of motor neurons can likewise lead to muscle degeneration and atrophy.

Calcium Control in Muscle Contraction

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Muscle Fibers, Tendons, and Contraction

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classification of skeletal muscle fibers

Skeletal Muscle Fiber Speed and Energy

Skeletal muscle fibers can be grouped by how fast they contract and how they make ATP, the energy cells use for movement. These differences also shape their physical features. Most human muscles contain all three fiber types, but in different amounts. Slow oxidative fibers, also called slow-twitch fibers, appear red because they have many capillaries and high levels of myoglobin, an oxygen-storing protein. They also contain more mitochondria, which make ATP through oxidative phosphorylation,...

muscle contraction

Nerve Signals That Trigger Muscle Contraction

Nerve signals trigger muscle contraction in both skeletal and smooth muscle, but the two muscle types use different control systems. In skeletal muscle, the signal begins at the motor end plate, which is the synapse between a motor neuron and a muscle fiber. In smooth muscle, contraction is controlled by the autonomic nervous system and happens without conscious control. In skeletal muscle, motor nerve terminals release acetylcholine. This neurotransmitter binds to receptors on the sarcolemma,...

cross-bridge cycle

Calcium control in muscle contraction depends on ATP, motor neurons, and the sliding action of actin and myosin. As a muscle contracts, the thin and thick filaments overlap more, and the sarcomere, which is the contractile unit of the muscle, becomes shorter. This process uses energy from ATP and happens in a repeating cycle at the molecular level. Myosin drives the movement of actin through a cross-bridge cycle. When ATP attached to the myosin head is hydrolyzed to ADP, myosin shifts into a...

motor units

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key terms and concepts

Learn how calcium, troponin, tropomyosin, and ATP control muscle contraction, from motor neuron signaling to relaxation and muscle degeneration.

Calcium Control in Muscle Contraction | JoVE K12

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Calcium Control in Muscle Contraction

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