Lecture 14

Question 1

skeletal muscle

Answer 1

attached to bone and tendon allowing it to move the body. multinucleated due to fused myoblast precursor cells and striations due to filaments. At NMJ, always excitatory. If muscle is relaxed, it’s due to absence of neurotransmitter (ACh).

Question 2

Epimysium

Answer 2

Sheath covering entirety of muscle that provides strength and elasticity

Question 3

Perimysium

Answer 3

Deep to epimysium. Similar structure and function but surrounds fascicle.

Question 4

Endomysium

Answer 4

Deep to perimysium. Envelops each myofibril.

Question 5

t-tubules

Answer 5

perforations that allows the extracellular fluid to be exposed along the myofibril allowing rapid depolarisation and repolarisation for coupling and contraction.

Question 6

skeletal muscle contraction structures

Answer 6

high [voltage-gates Ca channels] in t-tubules is associated with SR (increases [Ca] in SR). Allows low intracellular fluid conc. of Ca. You have stores of Ca that is only released when needed. During depolarisation at NMJ, influx of Ca occurs causing Ca dependent Ca release (rhinodine receptors on SR release more Ca)

Question 7

sarcomere

Answer 7

what lies between 2 adjacent z lines

Question 8

z-line

Answer 8

anchors thin filaments

Question 9

m-line

Answer 9

middle of sarcomere. Anchors thick filaments and contains cross-connecting elements of cytoskeleton

Question 10

interaction

Answer 10

heads of myosin interact with actin and ability to do so is cross-bridge cycling

Question 11

A-band

Answer 11

contains myosin fibres. Name given because of anisotropic property (appears different brightness based off angle light is shone). Doesn’t change length during contraction.

Question 12

I-band

Answer 12

No myosin. Actin only. Name given because of isotropic proterty (brightness doesnt’ change). shortens during contraction

Question 13

h-zone

Answer 13

h=hella (means brighter). contains myosin only and no actin overlap. Becomes smaller during contraction (increases overlap)

Question 14

molecular structure of striation and contractions

Answer 14

where myosin heads and globular actin molecules interact, ATP is hydrolysed which causes an increase in overlap and that’s the active components of contraction. Passive components (elastic) where titan anchors ends of each thick myosin filaments to z-line and acts like a rubber band. At optimal length which causes the greatest force of contraction (greatest overlap of actin and myosin) without stretching the elastin. Any further decreases capacity for active force as increases passive force.

Question 15

Nebulin

Answer 15

Middle of actin filament. Structural protein that provides a scaffold to anchor G-actin molecules.

Question 16

Troponin

Answer 16

Critical for the amount of binding (actin and myosin), ATP hydrolysis and cross bridge cycling

Question 17

Tropomyosin

Answer 17

Anchors troponin

Question 18

Thin filament structure

Answer 18

In relaxed state, no excitation of NMJ and low intracellular Ca. Conformational of this as troponin covers binding site of G-actin molecule, preventing cross-bridge cycling. During excitation, Ca binds to troponin causing conformational change in tropomyosin and troponin moves off binding site, allowing ATP hydrolysis and cross-bridge cycling.

Question 19

Thick filament structure

Answer 19

Anchored at midline so each individual myosin fibres has a tail, head and hinge region.

Question 20

Myosin head

Answer 20

has capacity for ATP hydrolysis and G-actin protein binding.

Question 21

Hinge region

Answer 21

Between tail and head. Region where conformational change occurs. It bends, drawing actin and myosin closer together, allowing for contraction.

Question 22

Excitation-contraction coupling

Answer 22

skeletal muscle is stimulated to contract by ACh release at NMJ. ACh binds to receptor-channels on the motor end plates of the muscle and sets off an action potential along the surface of the muscle fibre and t-tubules. T-tubules dip into muscle fibres and activate Ca release from intracellular SR stores into sarcomeres = contraction. In skeletal muscle, depolarisation of voltage gates Ca channels is directly coupled to rhinodine receptors on SR, but, in cardiac muscle there’s no direct contact as Ca channels allow Ca influx into cell which binds to rhinodine receptors and so on.

Question 23

cardiac muscle

Answer 23

striated uninucleated and branched.

Question 24

Intercalated discs

Answer 24

Has gap junctions for passage of small ions. Critical for passing over action potential to next cell.

Question 25

sinoatrial pacemaker cells

Answer 25

do not contain any contractile elements. They generate and initiate action potentials. Depends on the balance between ANS branches for rate of firing. When they initiate action potentials through intercalated discs, they can pass it onto contractile muscle which is passed onto the next.

Question 26

Rigour Mortis

Answer 26

After you die, SR break down, releasing all of it's Ca into the muscle. This causes stiffness as muscles are at maximum level of contraction possible. Stays like that until muscle fibres break down and return to relaxed state.

Question 27

muscle relaxation

Answer 27

can occur without death by pumping Ca into the SR using ATP and utilising the K/Na/ATP pump to pump Ca out of cell.

Question 28

SM

Answer 28

Doesnt' have sarcomeric arrangement of actin and myosin. Each myosin molecule is surrounded by 10-15 actin molecules (skeletal and cardiac is 1:1) and so, myosin chains are much longer that other muscle types. Contractile units run more-or-less parallel to the long axis of the cells. More eliptical in shape. You have CT connecting SM, dense bodies and intermediate filaments creating a general cytoskeletal structure. Actin attaches to dense bodies and between them, there's myosin. Myosin heads point in opposite direction in terms of contracting the actin. So, you're pulling one in one direction and the opposing one in the opposite direction. That causes a twisting mechanism of contraction which shortens the cell (also makes them look fat)

Question 29

Contraction in SM

Answer 29

1. intracellular Ca conc. increases when Ca enters cells and is released from SR 2. Ca binds to calmodulin. 3. Ca-calmodulin activates myosin light chain kinase 4. MLCK phosphorylates light chains in myosin heads and increases myosin ATPase activity 5. Active myosin crossbridges slide along actin and creates tension.

Question 30

Relaxation in SM

Answer 30

1. muscle is contracted 2. Free Ca in cytosol decreases when Ca is pumped out of the cell or back into SR 3. Ca unbinds from calmodulin. MLCK activity decreases 4. Myosin Phosphatase (MLCP) removes phosphate ion from myosin light chains which decreases myosin ATPase activity 5. Less myosin ATPase activity decreases muscle tension

Question 31

Single unit SM

Answer 31

Connected electrical transmitting gap junctions causing them to contract as a unit. Allows binding of ligand to one cell and through GJ, it is passed onto subsequent cells. GIT

Question 32

multi-unit SM

Answer 32

Cells activated independently. Varicosities release neurons that much reach each cell instead of the one. Eye

Question 33

Purpose of single or multi unit SM

Answer 33

Different modalities allow for different levels of control. In GIT, you dont need subtle adjustments like eye.

Question 34

Phasic contraction

Answer 34

In relaxed state in normal conditions. When it is activated, increases contraction e.g oesophagus

Question 35

Tonic contraction

Answer 35

contraction force is high in passive state and you relax it when activated e.g sphincters (relax to piss and shit)