Vertebrates 9 - Muscular

Question 1

Muscle function

Answer 1

Support, movement of body or materials in it, vocalization, heat is a by-product

Question 2

Smooth muscle

Answer 2

Looks smooth. Line the gut, bladder, blood vessels. Involuntary. Small, spindle-shape, mononucleate. Actin/myosin irregular arrangement.

Question 3

Striated muscle

Answer 3

Regular cytoskeleton protein arrangement. Cardiac and

Question 4

Cardiac muscle

Answer 4

Mononucleate or bi, separated by intercalated discs with gap junctions. Involuntary, myogenic contraction (autorhythmic)

Question 5

Skeletal muscle

Answer 5

Large, polynucleate cells = myofibers made from fusing myoblasts. Neurogenic contraction (needs nerve stimulus). Similar in all vertebrates.

Question 6

Structure of muscle

Answer 6

Muscle made of bundles of muscle fibers (cells), muscle fiber contains of bundles of myofibrils. Each segment of myofibril is a sarcomere

Question 7

Sarcomere

Answer 7

I band (Z line in middle holding thin filaments), A band, H zone (M line in middle holding thick filaments) Thin filaments have actin.

Question 8

Sliding filament theory (it’s proven)

Answer 8

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.

Question 9

Why do the myosin heads change shape when ATP binds?

Answer 9

Energy interferes with the bonds that create the 3º struture

Question 10

Proof for sliding filament theory study

Answer 10

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.

Question 11

Regulation of Contraction

Answer 11

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.

Question 12

Excitation-Contraction coupling

Answer 12

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.

Question 13

Motor unit

Answer 13

A motor neuron and all the muscle fibers attached to it.

Question 14

Innervation

Answer 14

In agnathans, not all of them are innervated, possibly “share”. All other vertebrates each muscle is innervated.

Question 15

Electromyography

Answer 15

Measure electrical activity in muscles with electrodes

Question 16

Latent period

Answer 16

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.

Question 17

Sarcoplasmic reticulum

Answer 17

Modified ER. Spread throughout the cells, and wraps all the way around the myofibrils. Not used in protein formation etc. Ca retention and release.

Question 18

Triad

Answer 18

One T tubules and two SRs that meet near the myofibrils.

Question 19

How are action potentials linked to contraction?

Answer 19

Calcium. Helps actin and myosin interact in contraction.

Question 20

Calsequestrin

Answer 20

Protein in the SR that binds Ca loosely. Helps regulate contraction

Question 21

How does SR regulate Ca?

Answer 21

Contain Ca pumps which are always on. Help reuptake of Ca

Question 22

Ryanodine receptors

Answer 22

Help in Ca movement. Found on SR membrane

Question 23

DHPR

Answer 23

Dihydro puridine receptor. Voltage gated ion channel. On T Tubule membrane.

Question 24

Steps to contraction

Answer 24

Depolarize T Tuble; change shape of receptors, Ca can leak out Ryano and DHPR. To stop we need to stop the nerve, everything repolarizes.

Question 25

Reading: what is PEPCK

Answer 25

Phosphoenolpyruvate carboxykinase. PEP is the precursor to pyruvate in glycolysis (but PEPKC works in the other direction)

Question 26

Reading: Roles and location of PEPKC

Answer 26

Involved in gluconeogenesis in the liver. Glyceroneogenesis in adipocytes (pyruvate/lactic acid made to fat)

Question 27

Reading: What does lactic acid do? Where from?

Answer 27

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)

Question 28

Reading: PEPCK experiment

Answer 28

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

Question 29

Reading: How to check that the PEPCK knock-in worked

Answer 29

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

Question 30

Reading: Phenotypic differences in the PEPCK mice

Answer 30

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.

Question 31

Reading: mechanism of the increased activity of the PEPCK mice

Answer 31

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)

Question 32

Reading: what implications do we have from the PEPCK experiment?

Answer 32

Potential to unlock the enzyme in humans, increasing endurance and in longevity