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Flashcards in Excitation of Skeletal Muscle Deck (18)
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1
Q

Neuromuscular Junction

A

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

2
Q

What is the neurotransmitter released from motor neurons?

A

Acetylcholine

3
Q

How is Acetylcholine (ACh)released?

A

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

4
Q

What happens after Acetylcholine is released from the motor neuron?

A

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

5
Q

How is the action potential spread to interior muscle cells?

A

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)

6
Q

Resting state of muscle cells

A

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)

7
Q

Voltage-Sensing Dihydropyridine (DHP) Receptor

A

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

8
Q

Ryanodine Receptor

A

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

9
Q

Sarcoplasm reticulum

A

ONLYsource of calcium for muscle cells

10
Q

Excitation-Contraction Coupling of muscle cells

A

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

11
Q

Relaxation of muscle cells after the excitation-contraction coupling

A

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)

12
Q

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

A

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

The choline is later added to Acetyl CoA = more ACh

13
Q

One propagationfrom the motor nueron produces…

A

…A muscle twitch

14
Q

How is the strength of muscle contraction increased?

A

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

15
Q

Drugs affecting skeletal muscle potential

A

Curariform drugs

Botulinum toxin

16
Q

Curare

A

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

17
Q

Botulinum Toxin

A

Neurotoxin produced by Clostridium botulinum

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

18
Q

Myasthenia Gavis

A

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