Excitable Cells Flashcards
action potential
rapid change in membrane potential
Resting membrane potential
slight negative charge inside cell
around -70mv
k+ leak channel
k+ moves down concentration gradient
outside of membrane becomes slightly positive
Na+ leak channel
Na+ moves down conc. grad. into cell
immediately removed by sodium potassium ATPase
equilibrium potential potassium
potassium stops moving when electrical gradient equal and opposite to concentration gradient
-86mv
sodium Eq
+60mv
- resting state
both voltage gated channels are closed
- slow rising phase
sodium moves through voltage gated channel
- rapid rising phase
sodium potassium ATPase moves through voltage gated channels
- early repolarisation
balance cant be reached so sodium channels blocked
- hyperpolarisation
potassium moved back into cell, channels blocked
describe movement of sodium ions as action potential is generated
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
describe movement of potassium ions as action potential is generated
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
How do voltage gated ion channels work?
activation gate is voltage dependent
inactivation gate is time dependent
open - inactivated - closed
absolute refractory period
membrane cannot generate another a.p. no matter how big the stimulus is
relative refractory period
membrane can generate another a.p if the stimulus is bigger than normal
where does the a.p. start?
axon hillock
how does axon diameter affect velocity of a.p.?
larger the diameter, the more room for local current flow in current loops
how does membrane resistance affect velocity of a.p.?
higher membrane resistance, less current lost by leaking as more current stays in current loops
multiple sclerosis
demyelination of axons so a.p. cannot jump between nodes of ranvier
gradual motor control loss
synaptic transmission
- a.p. invades axon terminal, presynaptic membrane depolarised
- depolarisation opens voltage gated Ca2+ channels
- Ca2+ rushes into axon terminal down conc. grad.
- rise in Ca2+ conc causes vesicles to fuse with presynaptic membrane
- vesicles release Ach into synaptic cleft (exocytosis)
- Ach molecules diffuse across cleft
- Ach molecules bind to receptors on postsynaptic membrane
- Ach molecules bind to receptor, ligand gated Na+ ion channels open
- Na+ rushes into postsynaptic cell, K+ leaves cell
postsynaptic MP is halfway between K+Eq and Na+Eq
ligand gated definition
opened by another molecule
e.g. ligand gated Na+ channels opened by Ach
end plate potential
halfway between Na+ Eq and K+Eq
-15mv
1 EPP
100 x mEPP
1 mEPP = 1 vesicle fusion
safety factor
abt 200-300 vesicles released even though only 100 needed for EPP
muscle fibre
many nuclei and mitochondria
contains many myofibrils
sarcomere
repeating unit within muscle fibre
thick filaments
proteins made of myosin
m line holds thick filaments together
thin filaments
made of actin, troponin and tropomyosin
g actin molecules
each g actin molecule has one myosin binding site
3 subunits of troponin
T, I, C
Ca2+ binds to C subunit, myosin binding site uncovered
T tubules
invaginations of muscle membrane (sarcolemma) penetrating deep into muscle fibres
sarcoplasmic reticulum
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
excitation contraction coupling
- myosin in high energy state
hydrolysed ATP to ADP+Pi - myosin heads rotate pulling thin filaments towards centre of sarcomere = powerstroke
- ATP binds to myosin head breaking actin-myosin bond and releasing ADP+Pi
- ATP is split returning myosin to its high energy state
all neurones…
- conduct electrical impulses and fire action ptentials
- communicate w neighbouring cells via synapses
- do not divide
graded potential definition
variable strength signals that travel over short distances and lose strength
occur in dendrites/cell bodies/axon terminals
size directly proportional to stimulus size
depolarising graded potential
EPSP
depolarising, closer to threshold
hyperpolarising graded potential
IPSP
drops below RMP
how do graded potentials interact w the axon hillock?
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
subthreshold EPSP
fails to reach threshold @ axon hillock
suprathreshold EPSP
just reaches threshold
divergence pathway
presynaptic neurone branches to affect large number of postsynaptic neurones called collateral axons
convergence pathway
large number of presynaptic neurones converge to affect a smaller number of postsynaptic neurones
spatial summation
EPSPs originate simultaneously at different locations on the neurone
postsynaptic inhibition
2 EPSPs can be diminished by summation with an IPSP
if the summed potential is subthreshold and no a.p. generated
temporal summation
graded potentials arrive at the same trigger zone close together in time
