CTB NTK for Final Flashcards
Inward currents promote ________. Outward currents promote _______.
Inward currents promote depolarization. Outward currents promote (re)polarization.
3 structural elements of ion channels
permeation module, gate module, and sensor module
muscle fiber surrounded by _____, fascicle surrounded by ______, whole muscle surrounded by ______.
fiber surrounded by endomysium, fascile by perimysium, muscle proper by epimysium
CapZ
binds to the barbed end of actin
Titin
large protein that creates an elastic connection between z discs
Nebulin
prevents actin polymerization
Dystrophin
stabilizes plasma membrane of skeletal muscle (mutated in muscular dystrophy)
What are the T-tubule Ca channels?
Dihydropyridine receptors (DHPR), they are voltage dependent and connect to RYR “feet” proteins that span the SR-T space
What protein spans the SR-T space and is responsible for Ca release from the SR?
Ryanodine receptor (RYR) “feet” proteins
What pumps Ca++ back into the SR?
SERCA (2 Ca pumped per ATP)
What are the 3 activation states of muscle?
Contracting (myosin walks along actin, requires ATP, activated by Ca), relaxation (proteins inhibit actomyosin interactions), and rigor (ATP depleted, no passive stretching)
Tropomyosin
blocks actin-myosin binding during relaxation
Troponin: TN-C, TN-I, and TN-T
TN-C binds Ca, TN-I inhibits actin-myosin interaction and TN-T binds tropomyosin.
Ca binds to TN-C –> conformational changes move tropomyosin out of myosin binding site and allow actomyosin binding
Advantages and disadvantages of longer muscles?
Advantages: greater shortening ranges and shortening rates. Disadvantage: require more ATP
Classifying muscle types
Type I: slow twitch (red) have smaller diameter, are fatigue resistant, have more myoglobin, and have lipid droplets.
Type IIa: moderately fast and red
Type IIb: fast twitch (white) have low mitochondria content and low oxidative enzyme content.
What is dystrophin?
The protein that transmits force of muscle contraction to ECM (in membrane), w/ homology to spectrin. It’s mutated/deficient in muscular dystrophy.
What are some symptoms of myesthenia gravis?
Weakness and fatigue in skeletal muscles, ptosis (droopy eyelids), diplopia (double vision), impaired speech, etc.
What causes MG? How to treat MG?
Caused by a problem in the NMJ – MEPPs are smaller (even w/ same amount of ACh). Treated w/ acetylcholinesterase inhibitors like prostigmin and mestinon
