Striated muscle contraction Flashcards
- Describe how rise in intracellular Ca leads to activation of the tropomyosin-troponin system and initiation of striated muscle contraction - Describe how activation of nicotinic receptors at the neuromuscular junction leads to contraction of skeletal muscle - Describe how activation of Beta1= adrenorececeptors leads to cardiac muscle contraction
Define cytosolic
Fluid portion of cytoplasm exclusive of organelles and membranes
What is the troponin system?
- Essential link between rise in Ca2+ and striated muscle contraction
What 3 protein subunits does the troponin complex system consist of?
- TnT
- TnI
- TnC
What does TnT do?
Binds to tropomyosin, forming the troponin-tropomyosin complex
What does TnI do?
Binds to active actin sites- prevents myosin-actin interactions
When calcium binds to TnC, the other part of TnC binds to TnI, and this leads to a conformational change that allows troponin to bind to tropomyosin
What does TnC do?
- Binds Ca2+
How is the tropomyosin-troponin system activated?
- By a rise in Ca2+
- Actin active sites are covered by tropomyosin held in place by troponin system (T,I,C)
- Ca2+ binds to Trop- C
- This induces a changing conformation of TnT-TnI- tropomyosin complex exposing actin active sites
- Allows myosin head to bind
- Initiates sliding filament hypothesis
What is the NMJ?
-Synaptic connection between the terminal end of a motor nerve and a muscle
How is skeletal muscle contraction initiated?
By activation of nicotinic ligand receptors by acetylcholine (Ach), this mediates communication between the motor nerve and skeletal muscle at the neuromuscular junction
How are nicotinic receptors activated at NMJ?
- An action potential is conducted in the motor nerves
- This activates VGCC and there’s an influx of Ca2+ ions
- Ca- dependent release of Acetylcholine, the acetylcholine is able to cross the synapse in vesicle
- Acetylcholine activates nicotinic ligand-gated receptors
- This generates an excitatory junction potential (EJP)
- This activates VgNa, these open allowing an influx of Na+ initiating an action potential - leads to depolarisation causing contraction
- Breakdown of Ach by AchE- termination of response
How does Ach-mediated EJP produce action potentials?
- Depolarisation inside musculoskeletal cells produces an EJP, which, when reaching the threshold value, activates VGNa, which causes depolarisation, hence producing an action potential.
What are RyR?
Receptors on SR which mediate Ca2+ release
They’re ligand- gated receptors
RyR1 receptors are on the SR
How is the contraction produced specifically at skeletal muscle?
- AP conducted to t- tubule, activates VGCCs
- Direct coupling between activated VGCCs and RyR on sarcoplasmic reticulum (SR)- RyR opens, causes release of Ca
- Ca binds to troponin C- allows actin-myosin interactions, as the conformation of the troponin C changes to remove tropomyosin from the actin active site
- Myosin heads perform power stroke (when ADP released from myosin head)
- Contraction- actin filaments move toward centre of sarcomere
What does the release of acetylcholine do?
- Generates an action potential, conducted to t-tubule.
- This activates VGCC
- Direct coupling between VGCCs and Ryanodine receptors (RyR) on sarcoplasmic reticulum (SR) causes the RyR to open, releasing calcium ions.
- Calcium ions binds to troponin C- this allows actin-myosin interactions
- Myosin heads perform power stroke
- Contraction- actin filaments move toward centre of sarcomere
How does cardiac muscle contract?
- The contraction of the heart is initiated by the action potential it is able to generate myogenically.
- Via activation of Beta1-adrenoreceptors, cardiac muscle can increase its contractions
