Striated muscle contraction Flashcards
What are the three subunits in the troponin system?
-TnT
-TnI
-TnC
What does TnT bind?
-TnT-binds to tropomyosin
What does TnI bind and what does this prevent?
-TnI-binds to active actin sites
-This prevents myosin-actin interactions
What does TnC bind?
-TnC-binds Ca2+
What happens to the tropomyosin-troponin system at resting Ca2+ levels?
-At Resting Ca2+ levels
-Actin active sites are covered by tropomyosin held in place by troponin system(T,I,C)
What happens to the tropomyosin-troponin system when Ca2+ levels rise?
-When Ca2+ levels rise:
-Ca2+ binds to TnC
-This changes conformation of TnT-TnI-tropomyosin complex exposing actin active sites
-This allows myosin head to bind
What does activation of nicotinic ligand gated receptors by Ach mediate? What does this initiate?
-Activation of nicotinic ligand gated receptors by acetylcholine(Ach) mediate communication between motor nerve and skeletal muscle at neuromuscular junction(NMJ)
-This initiates muscle contraction
Steps involved in activation of nicotinic receptors at NMJ in skeletal muscle?
- Conduction of action potential in motor nerves
- Activation of voltage-gated Ca2+ channels and Ca2+ influx
- Ca2+ dependent on release of Ach
- Ach activates nicotinic ligand-gated receptors
- Generation of excitatory junction potential(EJP)
- Activation of voltage-gated Na channels and this initiates action potential resulting in contraction
- Ach is broken down by AchE and this results in termination of response
In skeletal muscles, how does an Ach-induced action potential produce contraction?
- Action potentials conducted to t-tubule
a. This activates voltage gated calcium channels(VGCCs) - Direct coupling between VGCCs and RyR on sarcoplasmic reticulum(SR)
a. RyR opens and causes release of Ca2+ - Ca2+ bind to troponin C
a. This allows actin-myosin interactions - Myosin heads perform power stroke
- Contraction
a. This is due to actin filaments moving towards centre of sarcomere
Where is electrical activity generated in the heart and what is it conducted through to get to cardiac muscles?
-Electrical activity generated in Sino-atrial node(no nerve input required) is conducted through the heart to muscle cells
What does the electrical stimulation from the sinoatrial node lead to?
-The electrical stimulation leads to activation of cardiac action potentials
What do cardiac action potentials give rise to and what are the steps involved in this? What does this lead to?
- Action potential activates VGCC
- This activation causes Ca2+ influx
- Ca2+ will also bind to Ryanodine receptor(RyR) on the Ca2+ store which results in Ca-induced Ca release
- This results in a increase in intracellular Ca2+
- Ca2+ interacts with troponin system
- Leads to contraction
What is the G-protein coupled receptor, beta-1 adrenoceptor activated by and what does this increase?
-Although contraction of cardiac muscle is initiated by cardiac action potentials, activation of G-protein-coupled beta1-adrenoceptors is by noradrenaline released from sympathetic nerves and circulating adrenaline released from adrenal medulla
-This increases cardiac muscle contraction
How does stimulation of beta-1 adrenoceptors increase contraction of cardiac muscles?
- Noradrenaline or adrenaline will bind to beta1- adrenoceptors (GCPR)
a. Galphas pathway - This results in an increase in cAMP and PKA
- PKA will phosphorylate and activate VGCCs on cell membrane resulting in a Ca2+ influx
- PKA also phosphorylates RyR causes more Ca2+. Influx and more calcium induced calcium release
- This increase in calcium leads to activation of troponin
a. This increases contractility
How is cytosolic Ca2+ reduced to produce striated muscle relaxation?
-Ca2+ uptake into SR via Ca2+-ATPase
-Extrusion of Ca2+ from cell via Ca2+-ATPase and Na-Ca exchanger
