ICL 3.7: Physiology of Muscle Contraction

Question 1

how are muscles activated?

Answer 1

a somatic motor neuron splits into multiple axon terminals or terminal boutons

Question 2

what is a motor unit?

Answer 2

motor unit = all the muscle fibers innervated by a single motor neuron

larger nerve fibers have larger motor units and can do larger actions

Question 3

what are the steps of a skeletal muscle contraction?

Answer 3

1. action potential propagation in motor neuron via Na+
2. voltage gated Ca channels open
3. vessicles fuse with membrane and NTs are released into synaptic cleft
4. ACh binds to a chemically gated cation channel on the postsynaptic membrane
5. Na+ enters postsynaptic neuron at the motor end plate (specific part of sarcolemma)
6. depolarization of postsynaptic neuron
7. acetylcholinesterase breaks down ACh

Question 4

what’s another name for a nicotinic acetylcholine receptor?

Answer 4

ACh ligand gated Na/K channel

ACh is the ligand

Question 5

what is the structure of the acetylcholine-gated cation channel?

Answer 5

2 alpha subunits that each have to bind an ACh in order for the channel to open and Na+ to go in

the outside of the channel is also negatively charged so that Cl- can’t enter but Na+ will!

Question 6

what are the initial steps of a muscle contraction?

Answer 6

1. depolarization of skeletal fiber sarcolemma stimulates the DHP receptor, causing release of calcium from the sarcoplasmic reticulum
2. repolarization of the sarcolemma closes the calcium-release channel (ryanidine channel)
3. calcium ATPase pumps calcium back into the sarcoplasmic reticulum; calsequestrin collects calcium ions in the sarcoplasmic reticulum

Question 7

what is an isotonic contraction?

Answer 7

the same tone but the length of the muscle is changing

Question 8

what is an isometric contraction?

Answer 8

muscle tone changes but the length of the muscle doesn’t change

Question 9

what are the steps in a skeletal muscle contraction

Answer 9

1. calcium binds to troponin which causes a conformational change and the tropomyosin moves off of the myosin binding site of the actin
2. myosin binds to actin which causes a conformational change and myosin contracts
3. ADP+P are released
4. ATP comes in and binds to myosin and myosin releases from actin –> this is what explains rigor mortis because once you die, there won’t be any ATP to attach to myosin and get it to release from actin
5. ATPase immediately changes ATP into ADP+P

Question 10

how is multi-unit smooth muscle excited?

Answer 10

each individual multi-unit smooth muscle cell is innervated is by a neurotransmitter, which is either acetylcholine, norepinephrine or epinephrine

most of our smooth muscle is NOT like this; this is just in the eye and erector pili of the skin

Question 11

how is visceral smooth muscle excited?

Answer 11

visceral smooth muscle is excited by either a neural fiber, hormones, chemicals or stretch – a lot of things can effect smooth muscle contraction which is great!

when innervated by a nerve fiber, only the outer layers of a smooth muscle bundle is innervated by a neurotransmitter, which is typically either acetylcholine, norepinephrine or epinephrine –> in this method of activation, the excitatory stimulus travels to the inner layers by gap junctions

Question 12

what are the steps in smooth muscle contraction?

Answer 12

1. some stimuli opens Ca+2 channels and Ca+2 enters the smooth muscle

or the Ca+2 can be released from inside the sarcoplasmic reticulum via a secondary messenger

2. Ca+2 binds to calmodulin and activates myosin light chain kinase (MLCK)
3. activated MLCK adds phosphate to myosin and binds to actin
4. muscle contracts!

when the muscle wants to relax, the Ca gets pumped out of the cell into the extracellular fluid –> once ca levels drop to a certain point, myosin phosphatase removes phosphate from myosin and de-phosphorylated myosin is inactive

Question 13

what are all the steps of a muscle contraction?

Answer 13

1. an action potential in a motor neuron is propagated to the terminal button
2. the presence of an action potential in the terminal button triggers the opening of voltage-gated Ca+2 channels and the subsequent entry of the Ca+2 into the terminal button
3. Ca+2 triggers the release of ACh by exocytosis from a portion of the vesicles
4. ACh diffuses across the space separating the nerve and muscle cells and binds with receptor sites specific for it on the motor end plate of the muscle cell membrane
5. this binding brings about the opening of cation channels, leading to a relatively large movement of Na+ into the muscle cell compared to a smaller movement of K+ outward
6. the result is an end plate potential; local current flow occurs between the depolarized end plate and adjacent membrane
7. this local current flow opens voltage-gate Na+2 channels in the adjacent membrane
8. the resultant Na+2 entry reduces the potential to threshold, initiating an action potential which is propagated throughout the muscle fiber
9. ACh is subsequently destroyed by acetylcholinesterase, an enzyme located on the motor end plate membrane, terminating the muscle cells response