Excitation of Skeletal Muscle

Question 1

Neuromuscular Junction

Answer 1

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 2

What is the neurotransmitter released from motor neurons?

Answer 2

Acetylcholine

Question 3

How is Acetylcholine (ACh)released?

Answer 3

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 4

What happens after Acetylcholine is released from the motor neuron?

Answer 4

1) Acetylcholine attaches and stimulatesnicotinic receptorson Ligand (chemical) Gated Channelsonthe cell membranes of the muscle cells
2) Opening of these ligand gated channels allow for sodium to enter the cell
3) This causesend 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 5

How is the action potential spread to interior muscle cells?

Answer 5

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(extracellular fluid within T-tubules brings action potential to cells)

Question 6

Resting state of muscle cells

Answer 6

Resting membrane potential = -90mV

Low concentration of calcium within the cytoplasm of the cell

High concentration of calcium in theSarcoplasmic Reticulum

Calcium release channelclosed (Ryanodine Receptornot stimulated byVoltage-sensing dihydropyridine (DHP) receptors)

Question 7

Voltage-Sensing Dihydropyridine (DHP) Receptor

Answer 7

Receptor on cell membrane

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

“Uncorks”Calcium Release Channel(through stimulation of theRyanodine Receptor) causing release of calcium fromSarcoplasmic Reticulumto the cytoplasm of the muscle cell causing muscle contraction

Question 8

Ryanodine Receptor

Answer 8

Receptor oncalcium release channelsonsarcoplasmic reticulum

“Cork” of these channels

Stimulation fromvoltage-sensing dihydropyridine (DHP) receptorscauses “uncorking” of the ryanodine receptor which allows for the release of calcium from thesarcoplasmic reticuluminto the cytoplasm of the cell causing muscle contraction

Question 9

Sarcoplasm reticulum

Answer 9

ONLYsource of calcium for muscle cells

Question 10

Excitation-Contraction Coupling of muscle cells

Answer 10

1) Action potential from motor neuron travel to inner muscle cells alongtransverse T-tubules
2) Stimulation ofvoltage-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 totroponin Ccausing an actin myosin reaction
5) Muscle contraction occurs

High concentration of calcium in the cytoplasm of the cell

Question 11

Relaxation of muscle cells after the excitation-contraction coupling

Answer 11

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 calcium from troponn C)

Question 12

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

Answer 12

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

The choline is later added to Acetyl CoA = more ACh

Question 13

One propagationfrom the motor nueron produces…

Answer 13

…A muscle twitch

Question 14

How is the strength of muscle contraction increased?

Answer 14

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 15

Drugs affecting skeletal muscle potential

Answer 15

Curariform drugs

Botulinum toxin

Question 16

Curare

Answer 16

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 17

Botulinum Toxin

Answer 17

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 18

Myasthenia Gavis

Answer 18

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