Physiology - Excitation of Skeletal Muscle

Question 1

How is the strength of muscle contraction increased?

Answer 1

Neuron stimulation must be increased

Even though continuous depolarization and repolarization occurs in the muscle cell (i.e DHP opens and closes calcium release channels), calcium remains in the cytoplasm causing constant stimiulation and muscle contraction

Muscle contraction last longer and is stronger

Question 2

Sarcoplasm reticulum

Answer 2

ONLY source of calcium for muscle cells

Question 3

Ryanodine Receptor

Answer 3

Receptor on calcium release channels on sarcoplasmic reticulum

“Cork” of these channels

Stimulation from voltage-sensing dihydropyridine (DHP) receptors causes “uncorking” of the ryanodine receptor which allows for the release of calcium from the sarcoplasmic reticulum into the cytoplasm of the cell causing muscle contraction

Question 4

Excitation-Contraction Coupling of muscle cells

Answer 4

1) Action potential from motor neuron travel to inner muscle cells along transverse T-tubules
2) Stimulation of voltage-sensing dihydropyridine (DHP) receptors“uncorks” (Ryanodine receptors) calcium release channels on the sarcoplasmic reticulum
3) Calcium rushes into the cytoplasm of the muscle cells
4) Calcium binds to troponin C causing an actin myosin reaction
5) Muscle contraction occurs

High concentration of calcium in the cytoplasm of the cell

Question 5

Voltage-Sensing Dihydropyridine (DHP) Receptor

Answer 5

Receptor on cell membrane

Senses voltage (action potential) that propagates from motor neuron to T-tubules

“Uncorks” Calcium Release Channel (through stimulation of the Ryanodine Receptor) causing release of calcium from Sarcoplasmic Reticulum to the cytoplasm of the muscle cell causing muscle contraction

Question 6

What happens to Acetylcholine after it reacts with nicotinic receptors on skeletal muscle?

Answer 6

It gets broken down by Acetylcholinesterase (AChE) into acetyl and choline

The choline is later added to Acetyl CoA = more ACh

Question 7

What happens after Acetylcholine is released from the motor neuron?

Answer 7

1) Acetylcholine attaches and stimulates nicotinic receptors on Ligand (chemical) Gated Channels on the cell membranes of the muscle cells
2) Opening of these ligand gated channels allow for sodium to enter the cell
3) This causes end plate potential - either goes back to resting potential or threshold is reached causing depolarization (opening of voltage-gated sodium channels) to occur in the muscle cell

Question 8

Botulinum Toxin

Answer 8

Neurotoxin produced by Clostridium botulinum

Blocks release of ACh from nerve terminals = no fusion of ACh to nicotinic receptors = action potential not reached = paralysis

Question 9

One propagation from the motor nueron produces…

Answer 9

…A muscle twitch

Question 10

Drugs affecting skeletal muscle potential

Answer 10

Curariform drugs

Botulinum toxin

Question 11

Myasthenia Gavis

Answer 11

A disease characterized by skeletal muscle weakness

Believed to be autoimmune disease = antibodies present that block activation of nicotinic receptor = not as many activated = action potential not reached = paralysis

One treatment = acetylcholinesterase inhibitors (neostigmine) = ACh NOT broken down = so will hopefully attach to receptors due to increased concentration

Question 12

Neuromuscular Junction

Answer 12

Transmission of impulses from nerves to skeletal muscle fibers

Where the nerve and the muscle come together

The nerve innervates around the middle of the muscle and releases Acetylcholine to stimulate action potential and the cell membranes of muscle fibers

Question 13

Curare

Answer 13

Acts as an antagonist blocking nicotinic receptors and causing competition for ACh (agonist)

Not enough nicotinic receptors activated = not a high enough end plate potential = threshold not reached = no action potential = paralysis

competition is dependent on concentration and afinity of curare

The respiratory muscles are affected first

Question 14

Resting state of muscle cells

Answer 14

Resting membrane potential = -90mV

Low concentration of calcium within the cytoplasm of the cell

High concentration of calcium in the Sarcoplasmic Reticulum

Calcium release channel closed (Ryanodine Receptor not stimulated by Voltage-sensing dihydropyridine (DHP) receptors)

Question 15

How is the action potential spread to interior muscle cells?

Answer 15

The plasma membrane (Sarcolemma) continues into the muscle cell = T-Tubules (invaginations of the cell membrane

Action potential is spread by the way of transvers T-tubules

1) Extracellular fluid within T-tubules brings action potential to cells

2)

Question 16

How is Acetylcholine (ACh) released?

Answer 16

1) The action potential travels down the axon to the axon terminal of the motor neuron
2) Depolarization of the axon terminal causes Voltage-Gated Calcium Channels to open
3) Calcium rushed into the axon terminal
4) Calcium affects vesicles that contain Acteylcholine, which is then released from the axon terminal into the Synapse through exocytosis

Toxins that affect this pathway cause paralysis

Question 17

What is the neurotransmitter released from motor neurons?

Answer 17

Acetylcholine

Question 18

Relaxation of muscle cells after the excitation-contraction coupling

Answer 18

1) Skeletal muscle repolarizes
2) Calcium release channels are “replugged” (Ryanodine receptor) by voltage-sensing dihydropyridine receptor
3) Calcium gets pumped back in the sarcoplasmic reticulum lowering the amount of calcium in the cytoplasm of the cell (decrease of calcium in the cytoplasm of the cell causes release of calcum from troponn C)