Excitable Tissue : Muscle Flashcards
Tendons
Where most skeletal muscles begin and end.
Muscle Fibre Morphology
- begin and end in tendons
- each muscle fibre is a single multinucleated cell
- no communication between muscle fibres ( it can’t take a signal and recruit other cells to participate)
- each muscle fibre is conmprosed of multiple filaments which execute contraction
Sliding filament theory
still just a theory, best information we have to date about muscle contractions.
- has a handful of different proteins but MYOCIN generates contraction
all or nothing muscle contraction
we do not want this and our muscles are not designed for this. we don’t want to use max energy when we want to sharpen a pencil or do accupuncture. We have a graded muscle response.
Actin
Contractile Protein
Polymerizes to form a thin filament. (gives structure)
Tropomysosin
Contractile Protein
Binds to the thin filament.
Additional structural protein
Myosin 2
Contractile Protein
Globular motor protein that has the ability to create tension and allow for contraction.
- thought of as little elastics that stretch and snap back
Troponin
3 Subunits :
Troponin I :
Inhibitory
Binds actin and prevents actin/myosin association at rest.
Makes sure that they do not touch
Troponin T :
provides stability - allows binding to create an environment where contraction is possible
binds tropomyosin and helps position it on actin.
Troponin C:
calcium binding site
on/off switch. When Ca2+ is around , it binds to Troponin C and muscle wants to contact
If Ca2+ is not bound/present the relaxed strate is reinforced
Calcium (Storage in Muscle contractions)
Stored in the T-tubules. When the fibres need more Ca2+, it is released to create contraction.
Important to have storage for calcium b/c free calcium may cause harm.
Excitation Contraction Coupling
(Dihydropyridine DHPR receptor voltage gated) (red tube)
- physically or spatialling linked to the ryanodine receptor (RyR) in the sarcoplasmic reticulum (Pink tube)
Activation of DHPR causes conformational change in RyR causing Ca2+ release from the SR
Contrast to calcium induced / calicum release in cardiac muscle
T/F :
Is there a change in length of individual thin or thick filaments?
False : no change in length. Increased amount of overlap within the cell.
At rest, where are myocin heads?
Myocin heads bound to ADP and in relaxed position relative to the thin filament. No Ca2+ bound.
Where does Ca2+ bind when it gets into the cytoplasm?
Binds to troponin C which induces a confirmational change , and exposes myosin binding sites on actin.
Power stroke
Myosin heads move into position to bind actin and “flex” , which shortens the muscle fibre releasing ADP in the process.
How does ATP detach from actin?
ATP binds the empty site where ADP was released.
What does ATP hydrolization cause?
Causes myosin to return to the relaxed position.
When do muscle contractions repeat?
If there is sufficient calcium and ATP present, the process repeats.