what kind of channels are in membrane that exhibits passive membrane behavior?
what does this mean?
current flow across membrane of only voltage-independent "leak" channels
resulting voltage change: as predicted by Ohm's law, w/ delay b/c of capacitance
Vm returns directly to original value when current ends
what kind of channels are in membranes that show active properties?
membranes including voltage-dependent channels - conductances respond to changes in Vm, which is reflected in current value
how do excitable membranes show active behavior? what do they respond to?
respond to thrshold depolarization with an action potential: all or none, stereotyped sequence of Vm changes
what is automaticity? what cells exhibit this?
cells that spontaneously & rhythmically generate action potentials
excitable cells that're specialized to act as pacemakers do this
point on an action potential when:
- threshold for initiatino
- reversal of membrane polarity at the peak
- afterhyperpolairzaiton before turn to Vm resting value
what would the effect on depolarization of a membrane be if inward rectifiers close? why?
depolarization would be larger than expected b/c membraen conductance for K+ is reduced
what controls resting potential of Vm in a neuron?
leak K+ channel
what channels cause large spike in depolarization in a neuron?
opening of voltage-gated Na+ channels
at hte peak of an action potential in a neuron, which channels are open?
voltage-gated K+ channels begin to activate
Na+ channels inactivate
which channels repolarize the membrane? which phase?
voltage-gated K+ channels and leak K+ channels
what happens to the membrane to cause an action potential?
a strong enough stimulus depolairzes the membrane to threshold for an action potential initiation
result: rapid, lare depolarization
membrane then beings to repolarize
which channels dominate at rest of action potential?
once Vm is depolarized to the threshold, which channels are in action?
voltage-gated Na+ channels open, drive Vm toward VNa
these channels begin to inactivate soon aftr peak of depolairzation
voltage-gated K+ channels also activate, repolarize the membrane
which channels repolarize the membrane of an action potential
voltage-gated K+ channels
what does Vm approach during afterhyperpolarization? why?
because until voltage-gated K+ channels deactivate, K+ conductance is larger than it was in resting membrane, making Vm get close to Vk
what kind of event is an action potential? what does this mean?
all or none - a stronger suprathreshold stimulus would cause Vm to reach threshold value more quickly, but wouldn't change the shape of the subsequent action potential
what and when is the absolute refractory period?
right after action potential, it's impossible to initiate another one
some time is required for recently inactivated Na+ channels to de-inactivate before they can generate another action potential
period ends when full complement of Na+ channels has been de-inactivated
what is state of channels during relative refractory pd? how might this show?
some Na channels have de-inactivated, but most have not
during this pd, may see small-amplitude, shallow slope spikes of Na+ channels as they de-inactivate
when does the refractory period end?
when full complement of Na+ channels has been de-inactivated
then can launch full new action potential
how does action potential travel down a neuron's axon?
like a "wave" - action potential propagates down the axon
axon contains: leak K+ channels, voltage-gated and inactivating K+ and Na+ channels
1) voltage-gated Na+ channels open, Na+ enters cytoplasm, results in depolarization
2) depolarization spreads along membrane due to redistribution of charges per entry of uncompensated positive ions
3) per Na+ influx, K+ channels open, K+ exits cell through delayed rectifiers
membrane is repoalirzed, action potential terminated in that region
what do all excitable heart muscle cells have in common?
1) long phase of depolarization compared to neurons
2) prominent use of Ca2+ as the depolarizing charge carrier
are heart muscle cells usually depolarized or polarized? why?
b/c mechanical pumping action of heart relies on contractions that last hundreds of milliseconds
describe action potential of the ventricles
At rest, cells are polarized at about -90 mV; Kir channels dominant conductance
1) Phase 0: membrane depolarizes to threshold for action potential initiation; voltage-gated Na+ channels activated; rapid depolarization & upstroke
2) Phase 1: early/fast repolarization; Na+ channels inactivate
3) Phase 2: plateau; delayed opening of voltage-gated Ca2+ channels; voltage-gated K+ channels slowly activate
4) Phase 3: repolarization; K+ current builds via various voltage-gated K+ channels, and Ca2+ current diminishes as voltage-gated Ca2+ channels inactivate
5) Phase 4: diastole: begins after membrane returns to well-polarized resting potential
what causes ventricular caridac muscle cell to return to its resting potential?
combination of voltage-gated Ca2+ channels inactivaing & voltage-gated K+ channels activating
what are the different heart muscle cells, what is each responsible for?
pacemakers: impulse generation
His-purkinje: impulse propagation
"working" muscle: contraction
what is normal sequence of events in cardiac cycle?
1) RA pacemaker cells spontaneously fire in the SA node, initiate an action potential
2) depolarization spreads through the atria, results in atrial contraction & stimulation of the AV node and His-Purkinje fibers that innervate ventricles
3) initiation, spread of action potentials in the ventricles, produces contraction that pumps blood to rest of the body
what does an electrocardiogram (ECG) show?
what are the different parts of the line?
electrical activity of the various excitable cells & localization in the heart
1) 1st deflection: P-wave, depolarization of the atria, corresponds to Phase 0 of Atria
2) QRS complex, corresponds to Phase 0 of Ventricle
3) T-wave, corresponds to Phase 3 repolarization of ventricles
what is the Q-T interval?
how long is it, normally?
the duration of the ventricular action potential and contraction
<450 ms normally
what happens in a patient with long QT syndrome?
delayed, slow repolarization
can give rise to premature action potentials during Phase 3, without waiting for normal trigger from atria
can lead to dangerous arrhythmia, called torsade de pointes - ventricles contract in uncoordinated manner, independent of normal atrial rhythm; reduces pumping efficiency of heart
what kind of pathology is LQTS?
"channelopathy," pathology caused by mutation in a channel
what cardiac channel mutations have been linked to LQTS?
1) voltage-gated Na+ channel; mutations impair inactivation, result in relative large inward current during plateau phase & deplayed repolarization
2) 2 of the voltage-gated K+ channels of Phase 3; causes delays and slows repolarization
what happens in LQTS w/ overexpression of hERG?
hERG is a K+ channel; mutated G628S site in pore of the channel, reduces its conductance