Vertebrates 9 - Muscular Flashcards
Muscle function
Support, movement of body or materials in it, vocalization, heat is a by-product
Smooth muscle
Looks smooth. Line the gut, bladder, blood vessels. Involuntary. Small, spindle-shape, mononucleate. Actin/myosin irregular arrangement.
Striated muscle
Regular cytoskeleton protein arrangement. Cardiac and
Cardiac muscle
Mononucleate or bi, separated by intercalated discs with gap junctions. Involuntary, myogenic contraction (autorhythmic)
Skeletal muscle
Large, polynucleate cells = myofibers made from fusing myoblasts. Neurogenic contraction (needs nerve stimulus). Similar in all vertebrates.
Structure of muscle
Muscle made of bundles of muscle fibers (cells), muscle fiber contains of bundles of myofibrils. Each segment of myofibril is a sarcomere
Sarcomere
I band (Z line in middle holding thin filaments), A band, H zone (M line in middle holding thick filaments) Thin filaments have actin.
Sliding filament theory (it’s proven)
I band disappears when contracted, sarcomere shrinks. Thick filaments have myosin heads which walk along actin of thin filaments. ATP binds, myosin head unbinds, cocks and cleaves ATP and binds to actin, ADP and P unbind and myosin flexes.
Why do the myosin heads change shape when ATP binds?
Energy interferes with the bonds that create the 3º struture
Proof for sliding filament theory study
electron microscopy on living rabbit muscle. Labelled the myosin heads with gold (electron dense). With no ATP added the heads didn’t move, did move with ATP about 20nm.
Regulation of Contraction
Thin filament is actin wrapped with tropomyosin with troponin attached. Ca binds to sites on troponin which exposes the binding sites for myosin. Troponin will be saturated with enough Ca, strongest force.
Excitation-Contraction coupling
Neuromuscular junction. Open Ca channels, NT released into cleft by exocytosis, lots of surface area on the muscle side for receptors, receptors release Ach, causes action potential in muscle.
Motor unit
A motor neuron and all the muscle fibers attached to it.
Innervation
In agnathans, not all of them are innervated, possibly “share”. All other vertebrates each muscle is innervated.
Electromyography
Measure electrical activity in muscles with electrodes
Latent period
Time b/w action potential in muscle and muscle contraction. The action potential has to travel down T tubule and release Ca from sarcoplamsic reticulum.
Sarcoplasmic reticulum
Modified ER. Spread throughout the cells, and wraps all the way around the myofibrils. Not used in protein formation etc. Ca retention and release.
Triad
One T tubules and two SRs that meet near the myofibrils.
How are action potentials linked to contraction?
Calcium. Helps actin and myosin interact in contraction.
Calsequestrin
Protein in the SR that binds Ca loosely. Helps regulate contraction
How does SR regulate Ca?
Contain Ca pumps which are always on. Help reuptake of Ca
Ryanodine receptors
Help in Ca movement. Found on SR membrane
DHPR
Dihydro puridine receptor. Voltage gated ion channel. On T Tubule membrane.
Steps to contraction
Depolarize T Tuble; change shape of receptors, Ca can leak out Ryano and DHPR. To stop we need to stop the nerve, everything repolarizes.
Reading: what is PEPCK
Phosphoenolpyruvate carboxykinase. PEP is the precursor to pyruvate in glycolysis (but PEPKC works in the other direction)
Reading: Roles and location of PEPKC
Involved in gluconeogenesis in the liver. Glyceroneogenesis in adipocytes (pyruvate/lactic acid made to fat)
Reading: What does lactic acid do? Where from?
Made from pyruvate when there is no oxygen. Leaks out of cell, changes pH and affects muscle activity. Goes through blood to liver, gluconeogenesis (Cori Cycle)
Reading: PEPCK experiment
Turn on PEPCK in skeletal muscle. Knock-in PEPCK gene with skeletal muscle actin promoter to be expressed in muscle; insert into stem cells, put into embryo, implant into surrogate mother, next generations will have the gene in their germ line
Reading: How to check that the PEPCK knock-in worked
Western blot using antibodies to show which tissues have that protein. WT only liver and kidney, no heart or skeletal muscle; +/+ also in skeletal muscle
Reading: Phenotypic differences in the PEPCK mice
Ate way more but stayed slimmer. Why? They were more active and burned it off. Huge endurance difference. Also, they aged slower and were fertile longer. And more aggressive.
Reading: mechanism of the increased activity of the PEPCK mice
Higher mito. count, but ATP isn’t usually limiting. Lactic acid was much lower, which means their Cori cycle to recycle it is more active (ie in the muscles)
Reading: what implications do we have from the PEPCK experiment?
Potential to unlock the enzyme in humans, increasing endurance and in longevity
