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physiology and anatomy > week 3: 10.4 > Flashcards

week 3: 10.4 Flashcards

1
Q

typical resting membrane potential in unstimulated neurons and skeletal muscle fibers

A

-70mV
-85mV

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2
Q

what is the membrane potential

A

measure of cellular polarisation that compares the cytoplasmic membrane surface charge to the extracellular surface charge

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3
Q

depolarisation

A

influx of sodium ions leads to depolarisation as membrane potential becomes less negative

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4
Q

hyperpolarisation

A

movement of potassium ions out of a cell leads to hyperpolarisation as membrane potential becomes more negative

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5
Q

repolarisation

A

return to resting potential

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6
Q

what do neurons and skeletal muscle fibres have

A

electrically excitable membranes

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7
Q

what do excitable membranes permit

A

rapid communication between different parts of a cell

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8
Q

what does depolarisation and repolarisation cause in neurons and skeletal muscle fibers

A

action potential (electrical impulse)
that is propigated along their plasma membranes

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9
Q

what do excitable membranes contain

A

voltage-gated ion channels

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10
Q

what are voltage gated ion channels activated and inactivated by

A

changes in membrane potential

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11
Q

when do the electrical channels become activated

A

when the membranes of neurons and skeletal muscle fibers first depolarise from resting potential to threshold potential

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12
Q

threshold potential of neurons

A

-60mV

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13
Q

threshold potential of skeletal muscle fibers

A

-55mV

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14
Q

upon reaching threshold potential,

A

voltage-gated sodium ion channels open and there is a rapid influx of positively charged sodium ions into a cell

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15
Q

what causes the closure of the voltage gated sodium ion channels

A

depolarisation peaks at a membrane potential of +30mV

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16
Q

how does repolarisation of membrane begin

A

voltage-gated potassium ion channels open and positively charged potassium ion leave the cell

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17
Q

what causes the membrane potential to become negative again

A

the loss of the more positive charges than entered the cell

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18
Q

what happens during refractory period

A

former conc of sodium and potassium ions across cell are restored through sodium-potassium ion pumps

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19
Q

why does action potential travel in one direction

A

Further depolarisation cannot occur until the refractory period is over
prevents action potential propagating back from where it came from

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20
Q

skeletal muscles fibers cannot begin contracting until,

A

they recieve instructions from motor neurons of the CNS

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21
Q

how do motor neurons carry instructions

A

in the form of action potentials

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22
Q

when does a contraction of a skeletal muscle fiber begin

A

sarcoplasmic reticulum releases stored calcium ions into the cytosol of the muscle fiber

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23
Q

when does a skeletal muscle fiber contraction end

A

as the intracellular calcium ions are reabsorbed

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24
Q

neuromuscular junction

A

synapse of a skeletal muscle fiber and a neuron

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25
Q

what is the NMJ made up of

A

axon terminal
motor end plate
synaptic cleft (in between)

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26
Q

what is the motor end plate

A

specialised region of the sacrolemma

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27
Q

what is a neurotransmitter

A

a chemical released by a neuron to change the permeability or other properties if another cell’s plasma membrane

28
Q

what does the cytoplasm of the axon terminal contain

A

vesicles filled with molecules of ACh

29
Q

what does the synaptic cleft and motor end plate contain

A

molecules of the enzyme AChE which breaks down ACh

30
Q

what is the synaptic cleft

A

narrow space that separates the axon terminal of the neuron from the opposing motor end plate

31
Q

what is the stimulus for ACh release

A

arrival of action potential at the axon terminal

32
Q

what happens when AP reaches neurons axon terminal

A

permeability changes in its membrane, triggers the exocytosis of ACh into synaptic cleft

33
Q

exocytosis occurs as,

A

vesicles fuse with the neruron’s plasma membrane

34
Q

once ACh is released into synaptic cleft,

A

diffuse across synaptic cleft
bind to ACh receptor membrane channels

35
Q

what does ACh binding to ACh receptor channels cause

A

opens the membrane channel on the surface of the motor end plate

36
Q

sodium ions movement and why

A

sodium ions rush into the cytosol
becuase extracellular fluid contains high conc of sodium ions and sodium ion conc inside cell is vey low

37
Q

what results in the generation of the action potential in the sarcolemma

A

sudden inrush of sodium ions

38
Q

how is ACh removed from the synaptic cleft

A

diffuses away from synapse
or
broken down by AChE

39
Q

what is ACh broken down into by AChE

A

acetic acid and choline

40
Q

why is the removal of ACh important

A

leads to the closing of ACh receptor membrane channels

41
Q

excitation contraction coupling

A

link between the generation of action potnetial in sacrolemma and the start of a muscle contraction

42
Q

where does the excitation contraction coupling occur

A

at the triads

43
Q

what happens when action potential reaches a triad

A

triggers the release of Ca2+ from the terminal cisternae of the sarcoplasmic reticulum

44
Q

how long does the change in permeability of the SR to Ca2+ last

A

0.03 seconds

45
Q

[Ca2+] in and around sarcomere after AP reaches triad

A

100 times resting level

46
Q

why is the effect of calcium ion release almost instantaneous

A

because terminal cisternae are loacted at zones of overlpa where thick and thin filaments ineract

47
Q

calcium ions binding to troponin

A

changes the shape of the troponin molecule
weakens the bond between troponin and actin
troponin molecule changes position rolling the attached tropomyosin strand away from the active sites
contraction cycle begins

48
Q

contraction cycle

A

series of molecular events that enable muscle contraction

49
Q

after active sights are exposed

A

myosin heads bind to them forming cross bridges

50
Q

connection between head and tail

A

functions as a hinge that leads the head pivot
pivots using energy released from hydrolysis of ATP
head swings towards the M line-power stroke
pivoting is the key step in muscle contraction

51
Q

what is the power stroke

A

when the head swings towards the M line

52
Q

what happens when muscle cells contract

A

they pull on the attached tendon fibers

53
Q

what type of force is tension

A

active- energy must be expended to produce it

54
Q

what must applied tension overcome before movement can occur

A

the objects load (or resistance)

55
Q

what is an objects load/ resistance

A

a passive force that opposes movement

56
Q

what does the load of an object depend on

A

weight, shape, friction ect

57
Q

when does the object move

A

when applied tension exceeds the load

58
Q

what is compression (force)

A

push applied to the object, tends to force object away from source of compression

59
Q

no movement can occur until applied compression,

A

exceeds load of object

60
Q

why can muscle cells pull but not push

A

muscle cells can use energy to shorten and generate tension through interaction between thick and thin filaments, but not to lengthen and generate compression

61
Q

what does each power stroke result in

A

sarcomere shortened by 0.5 %

62
Q

why does the entire muscle shorten at the same rate

A

all the sarcomeres contract together

63
Q

what does the speed of the sarcomere shortening depend on

A

the cycling rate- the number of power stroeks per second

64
Q

relationship between load and cycling rate

A

the greater the load, the slower the cycling rate

65
Q

duration of contraction depends on

A
  1. period of stimulation at NMJ
  2. presence of free calcium ions in cytosol
  3. availability of ATP
66
Q

contraction will continue if

A

additional action potentials arrive at NMJ in rapid sucession

67
Q

what does a series of action potentials arriving at the NMJ causing the continual release of ACh produce

A

series of action potentials in the sarcolemma that keeps Ca2+ levels elevated in cytosol

physiology and anatomy (31 decks)

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