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Cell Biology > Excitable Cells > Flashcards

Excitable Cells Flashcards

1
Q

action potential

A

rapid change in membrane potential

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2
Q

Resting membrane potential

A

slight negative charge inside cell

around -70mv

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3
Q

k+ leak channel

A

k+ moves down concentration gradient

outside of membrane becomes slightly positive

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4
Q

Na+ leak channel

A

Na+ moves down conc. grad. into cell

immediately removed by sodium potassium ATPase

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5
Q

equilibrium potential potassium

A

potassium stops moving when electrical gradient equal and opposite to concentration gradient
-86mv

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6
Q

sodium Eq

A

+60mv

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7
Q
  1. resting state
A

both voltage gated channels are closed

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8
Q
  1. slow rising phase
A

sodium moves through voltage gated channel

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9
Q
  1. rapid rising phase
A

sodium potassium ATPase moves through voltage gated channels

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10
Q
  1. early repolarisation
A

balance cant be reached so sodium channels blocked

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11
Q
  1. hyperpolarisation
A

potassium moved back into cell, channels blocked

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12
Q

describe movement of sodium ions as action potential is generated

A

sodium ions enter cell, they would continue to do so until Eq is reached (+60) however channels inactivate at around +30 and block the ions from entering the cell

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13
Q

describe movement of potassium ions as action potential is generated

A

potassium ions continue to leave the cell even after repolarisation. Rmp tries to reach the potassium Eq (-86mv) but potassium channels inactivate before it can reach this point

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14
Q

How do voltage gated ion channels work?

A

activation gate is voltage dependent
inactivation gate is time dependent
open - inactivated - closed

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15
Q

absolute refractory period

A

membrane cannot generate another a.p. no matter how big the stimulus is

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16
Q

relative refractory period

A

membrane can generate another a.p if the stimulus is bigger than normal

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17
Q

where does the a.p. start?

A

axon hillock

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18
Q

how does axon diameter affect velocity of a.p.?

A

larger the diameter, the more room for local current flow in current loops

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19
Q

how does membrane resistance affect velocity of a.p.?

A

higher membrane resistance, less current lost by leaking as more current stays in current loops

20
Q

multiple sclerosis

A

demyelination of axons so a.p. cannot jump between nodes of ranvier
gradual motor control loss

21
Q

synaptic transmission

A
  1. a.p. invades axon terminal, presynaptic membrane depolarised
  2. depolarisation opens voltage gated Ca2+ channels
  3. Ca2+ rushes into axon terminal down conc. grad.
  4. rise in Ca2+ conc causes vesicles to fuse with presynaptic membrane
  5. vesicles release Ach into synaptic cleft (exocytosis)
  6. Ach molecules diffuse across cleft
  7. Ach molecules bind to receptors on postsynaptic membrane
  8. Ach molecules bind to receptor, ligand gated Na+ ion channels open
  9. Na+ rushes into postsynaptic cell, K+ leaves cell
    postsynaptic MP is halfway between K+Eq and Na+Eq
22
Q

ligand gated definition

A

opened by another molecule

e.g. ligand gated Na+ channels opened by Ach

23
Q

end plate potential

A

halfway between Na+ Eq and K+Eq

-15mv

24
Q

1 EPP

A

100 x mEPP

1 mEPP = 1 vesicle fusion

25
Q

safety factor

A

abt 200-300 vesicles released even though only 100 needed for EPP

26
Q

muscle fibre

A

many nuclei and mitochondria

contains many myofibrils

27
Q

sarcomere

A

repeating unit within muscle fibre

28
Q

thick filaments

A

proteins made of myosin

m line holds thick filaments together

29
Q

thin filaments

A

made of actin, troponin and tropomyosin
g actin molecules
each g actin molecule has one myosin binding site

30
Q

3 subunits of troponin

A

T, I, C

Ca2+ binds to C subunit, myosin binding site uncovered

31
Q

T tubules

A

invaginations of muscle membrane (sarcolemma) penetrating deep into muscle fibres

32
Q

sarcoplasmic reticulum

A

tubular structure that surrounds the myofibrils enlarging terminal cisternae near the t tubules
get a.p. into parts of muscle that other membrane cant reach
a.p. in t tubules triggers Ca2+ release from TCs of SR

33
Q

excitation contraction coupling

A
  1. myosin in high energy state
    hydrolysed ATP to ADP+Pi
  2. myosin heads rotate pulling thin filaments towards centre of sarcomere = powerstroke
  3. ATP binds to myosin head breaking actin-myosin bond and releasing ADP+Pi
  4. ATP is split returning myosin to its high energy state
34
Q

all neurones…

A
  • conduct electrical impulses and fire action ptentials
  • communicate w neighbouring cells via synapses
  • do not divide
35
Q

graded potential definition

A

variable strength signals that travel over short distances and lose strength
occur in dendrites/cell bodies/axon terminals
size directly proportional to stimulus size

36
Q

depolarising graded potential

A

EPSP

depolarising, closer to threshold

37
Q

hyperpolarising graded potential

A

IPSP

drops below RMP

38
Q

how do graded potentials interact w the axon hillock?

A

pass through neurone until they die out or reach the axon hillock
if they depolarise the membrane t the threshold voltage an a.p. is initiated

39
Q

subthreshold EPSP

A

fails to reach threshold @ axon hillock

40
Q

suprathreshold EPSP

A

just reaches threshold

41
Q

divergence pathway

A

presynaptic neurone branches to affect large number of postsynaptic neurones called collateral axons

42
Q

convergence pathway

A

large number of presynaptic neurones converge to affect a smaller number of postsynaptic neurones

43
Q

spatial summation

A

EPSPs originate simultaneously at different locations on the neurone

44
Q

postsynaptic inhibition

A

2 EPSPs can be diminished by summation with an IPSP

if the summed potential is subthreshold and no a.p. generated

45
Q

temporal summation

A

graded potentials arrive at the same trigger zone close together in time

Cell Biology (7 decks)

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