Skeletal Muscle Pt2 Flashcards
Contraction of motor unit initiated from
CNS, occurs as all or noting twitch response
Contraction of motor unit steps
- Alpha-motor neuron propagates actio potential to muscle
- Acetylcholine released, binds at muscle endplate
- Channels in nicotinic receptors open -> Na+ diffusion into cell
- depolarization at motor endplate
- If enough miniature endplate potentials -> full fledged end plate potential
- Voltage gated Na+ channels open -> self propagating action potential spreads involving entire plasma membrane including T-tubule system membrane invaginations
- Voltage gated Ca2+ channels in T-tubules open
- Voltage-induced confrontational change t-tubule channel -> Ca2+ release channels opening
- Ca2+ flows out SR through release channels
- Large rapid increase in cytoplasmic calcium concentration
- Ca2+ binds troponin C
- Conformational change in troponin complex -> change troponin complex
- Conformatinal change troponin complex pulls tropomyosin out of normal position on actin
- myosin heads bind acting forming cross-bridges
- myosin head hydrolyzes ADP uses energy ATP hydrolysis to walk along actin filament
- Ca2+ removed from cytoplasm by Ca2+-ATPase of SR membrane
- Cytosolic Ca2+ concentration decreases
- Ca2+ released from troponin C
- Tropomyosin returns to resting portion blocking myosin binding sites on actin filaments
acetyl choline released from____ at ____
-released from presynatptic alpha-motor neuron at neuromuscular junction
acetylcholine diffuses across____ to bind to ____ in ___
acetylcholine diffuses across synaptic cleft to bind at nicotinic acetylcholine receptors in the muscle endlplate
nicotinic Ach receptors are
ligand-gated ion channels
Depolarization event at motor endplate is NOT
an action potential
action potenital occurs only if
enough miniature end plate potentials to summate to full-fledged end plate potential
Voltage gated Ca2+ channels in T-tubules closely associated with
calcium release channels in SR membrane which is why voltage-induced conformational change in T-tubule channel causes Ca2+ release channel to open
the linkage between voltage gated Ca2+ channels and Ca2+ release channels in SR is
- mediated direct mechanical interactions between channels on T-tubule and SR
- specifically by large cytoplasmic extension (foot process) of Ca2+ release channel
conformational change in troponin fx
- pulls tropomyosin out of normal position on actin allowing for interactions between actin and myosin
myosin heads biding actin form
cross bridges
single step of movement down actin filament produced by
each cycle of ATP binding, hydrolysis, and phosphate release
cross-bridge cycle continues until
Ca2+ removed from cytoplasm by Ca2+-ATPase of SR membrane (SERCA) ultimately leading to Ca2+ release from troponin C -> tropomyosin returning to resting position -> blocking myosin bing sites on actin filaments
sequence of events in excitation-contraction coupling
- action potential
- increase cytosolic Ca2+ concentration
- Muscle contraction
summation
- duration of contraction (twitch) long releative to duration exciting action potential so can initiate second action potential before first fully subsides causing second twitch to superimpose on residual tension first twitch this = summation
- if frequency stimulation great enough individual twitches occur v close together in time and then are no longer distinguishable from each other
ATP use muscle contraction
- Cross-bridge cycling
- moving Ca2+ from cytoplasm back into SR
- myocytes use ATP maintain and replenish membrane potentials
- in exercise muscle use ATP can exceed 100x basal rate
ATP needed for contraction and relaxation
small ATP stores so have to regenerate ATP needed in contraction and relazation
energy pathways in muscle fiber
- stores ATP and phosphocreatinin
- Anerobic glycolysis
- Oxidative phosphorylation
Phosphocreatinin
- most available pool energy= high energy bond phosphocratinine
phosphocreatinin produced by/ steps use
- transfer high energy phosphate from ATP to creatinine by creation kinase in mitochondria
- Phosphocreatinin diffuses from mitochondria -> major sites ATP utilization
- Phosphate transferred from phosphocreatinin to ADP
- dephosphorylated creatinine diffuses back to mitochondria where can be rephosphorylated