Skeletal Muscle Flashcards
Connective Tissue Layers
- Connective tissue layers: (**all 3 layers are cont and blend at myotendinous junction)
- Epimysium - surrounds whole skeletal muscle
- Perimysium - surrounds ea fasicles
- Endomysium - surrounds individual myofibers
Myofiber
Myofibril
Myofilament
W/in ea myofiber are multiple myofibrils which contain bundles of myofilaments (actin and myosin)
Myofiber = skeletal muscle cell= fiber
Sarcolemma (+3 special features)
- muscle fiber’s plasma membrane
1- DAPC (protein complex that links ECM w/ actin cytoskeleton)
2- Transverse tubules - thin invaginations in sarcolemma that is associated w. 2 sarcoplasmic ret networks to propagate depolarization of cell to inner fiber for Ca++ release
3 - Basement Membrane - collagen, laminins, agrin, etc
Sarcoplasmic Reticulum (+2 special features)
- mediates Ca++ release and uptake
- Form sacs on ea side of T tubules –> triads (2 sarcoplasmic ret sacs w/ 1 t tubule) for excitation-contraction coupling
- Contains Ca-ATPase to move ions from cytoplasm –> SR lumen for muscle relaxation
2 Types of Receptors
- Dihydropyridine (DHRP)- sense depolarization from T tubules; connect T tubules to sarcoplsamic ret; voltage-sensitive so voltage –> conformational change that then activates ryanodine receptors
- Ryanodine receptors - SR release channels; for release of Ca++ from SR –> cytoplasm/sarcomeric space –> myosin/actin interaction
- Calcium now able to bind to troponin C –> pulls tropomyosin in tighter so no longer blocking myosin binding site
Sarcomere Components (5)
- A-band is width of thick/myosin filaments
- H Zone - in center of A band; lighter and ONLY myosin
- M-line in center of H zone of A band; prod by links of thick filaments
- I band is just actin connected to the Z disc (alpha-actinin)
- Sarcomeres are connected at Z lines/Z discs (alpha-actinin)
Titan
filament attached to myosin to restore shape after contraction; spring-like
Satellite Cell and Nuclei
Nuclei are on periphery; if inc in muscle fiber length and nuclei no longer sufficient, satelittle cells will divide so one daughter cell can be used to inc # nuclei in nuclear domain
Hypertrophy v. Atrophy v. Hyperplasia
- Hypertrophy - inc in myofiber size/diameter
- Atrophy - dec in myofiber diameter
- Hyperplasia - inc # myofibers (only in animals and human smooth muscle)
Myosin Organization
- 2 heavy chains and 4 light chains
- Tail is just heavy chains
- Head is heavy and light chains; binds actin; has ATPase; on outside
- Forms filaments along w/ associated proteins
- C protein and M protein - connect thick filaments to ea other at M line
- Titan is filament attached to myosin to restore shape after contraction; spring-like
- Creatine Kinase - uses phosphocreatine to re-phosphorylate ATP
Actin Organization
- 2 helices of actin polymers wrapped around ea other
- Regulated by 2 proteins
- Tropomyosin- covers actin’s binding site for myosin head
- Troponin C – Ca+2 binding ***
- Troponin I – binds actin & troponin C
- Troponin T – binds tropomyosin to troponin C
4 Steps of Sliding Filament Theory
- 1- Myosin head bound to actin
- 2- ATP binds myosin head causing release from actin
- 3- Hydrolysis of ATP causes change in myosin that displaces it along actin by 5nm
- 4- Myosin now loosely bound at new position on actin; then phosphate released –> tight binding –> power stroke (myosin loses the bound ADP during stroke)
What is a motor unit?
- If need greater strength then recruit more motor units
- Motor unit = 1 axon, mult NMJs, all muscle fibers innervated by them
Muscular Dystrophy
can be caused by mutations in proteins of the dystrophin-associated protein complex (DAPC)
Malignant Hyperthermia
- genetic defect in ryanodine receptor –> uncontrolled release of Ca++ from SR –> rigid muscles and inc metabolic state –> hyperthermia and muscle damage
- Usually notice when given anesthesia
- Treat w/ Daltrolene - muscle relaxant that works directly on ryanodine receptors
Corticosteroid Myopathy
- chronic admin of corticosteroids –> proximal muscle weakness and atrophy; usually improves if discontinue med
Role of Ca++ In Smooth Muscle
- no t tubules; myosin is globular at rest then Ca++ –> Ca-calmodulin –> activates myosin light chain kinase –> phosphorylates myosin light chain –> transiently becomes a filament; Ca-calmodulin also binds caldesmon to remove it from myosin binding site on actin
- Relaxation … Ca++ removal (Ca ATPases or Ca exchanger) AND myosin light chain phosphatase
How can smooth muscle sustain tonic contraction?
- stay contracted w/o expending ATP
- Rho-kinase inactivates myosin light chain phosphatase so myosin stuck in filament form
