muscle physiology 2 Flashcards
What starts each contraction/power stroke?
Ca+ increases intracellularly
what happens when Ca+ increases intracellularly?
- Ca2+ binds troponin
- troponin rotates and causes the displacement of tropomyosin
3.Binding sites on actin are now available
which ATPase model do we use? what is it?
Huxley
what causes myosin to release actin?
ATP attachment
what are the activation steps? (starting from ACh being released)
- Somatic motor neuron releases ACh at neuromuscular junction
- Na+ enters through ACh receptor channel initiates muscle AP
- AP in t-tubule changes conformation of Dihydropyridine (DHP) voltage receptor
- DHP receptor opens the Ca+ release channels in SR and Ca+ enders cytoplasm
- Ca+ binds to troponin allowing actin/myosin binding
- Myosin heads execute power stroke
- Actin filament slides to center of sarcomere
_______ sits at the junction between the I and A band and maintains SR Ca+ storage
T-tubule
what is inside T-tubules?
Extracellular (interstitial) fluid inside T tubules
________ sit on either side of the T-tubule
Lateral sacs/cisternae
________ + ______ = triad
T-tubule, 2 lateral sacs
_______ receptors are on lateral sac and ______ receptor on T-tubule
Ryanodine
DHP
_________ helps to reduce Ca gradient when you pump it back into SR, it makes the ATPase pump work more efficiently
Calsequestrian
how many Ca+ does Calsequestrian bind?
~43
what are the sequence of events in contraction? (starting at discharge of neuron)
- Discharge of neuron
- ACh release at motor end plate
- ACh binds nicotinic receptors
- Increase Na/K conductance
- Generation of endplate potential
- Generation of AP on sarcolemma
- Generation of AP in T-tubules
- SR (cisternas) release Ca+
9.Ca+ binds troponin, which displaces tropomyosin - Crossbriges form, then powerstroke, then shortening
- Ca+ actively taken up by SR when there is no longer an AP
- Tropomyosin slips back to its blocking position on actin, contraction ends, actin slides back to original resting position
where are these channels located?
1. Chemical gated ACh receptor
2. Voltage gated Na+ channels
3. Voltage gated Ryanodine, DPH
- end plate
- sarcolemma
- sarcoplasmic reticulum
bringing Ca+ back to SR goes _____ its concentration gradient
against
what are the sequence of events in relaxation?
- Ca actively pumped back into longitudinal membranes of SR, moved to cisterns, and bound to Calsequestrin (43 Ca+)
- Ca+ leaves troponin down a concentration gradient
- Tropomyosin and troponin move back into blocking position
- Cessation of actin + myosin interaction
what are the 3 things ATP is used for during contraction?
- Energy for power stroke
- Energy for release of myosin head from actin
- Ca+ pumps on SR (~30% ATP for a single twitch)
____________ is the process by which depolarization of muscle fiber initiates contraction
Excitation-Contraction Coupling
Electrical activity lasts about ______ while Mechanical activity lasts _______ and can start before electrical stimulation is over
1-2ms, ~7.5-100ms
what type of fibers are at a motor end plate?
large myelinated A-alpha
which neurotransmitter causes depolarization?
ACh
______ breaks down ACh
acetylcholinesterase
where are motor end plates located? why?
Located in middle of fiber so depolarization can spread evenly
what are the steps at a motor end plate? (starting with AP coming down neuron)
- AP comes down motor neuron
- Voltage gated Ca+ channel opens
- Vesicles fuse and neurotransmitter (ACh) released out
- ACh binds to nicotinic receptors on postsynaptic membrane
- Na can now come in and K+ can leave → depolarization
- Depolarization of areas next to endplate lead to AP that spreads over sarcolemma
