chap 5- membrane & action potentials (b1- SMS) Flashcards
what is membrane potential?
difference in electrical charge (voltage) between the inside and outside of a cell, due to the uneven distribution of ions across the cell membrane
- inside (ICF): slightly negative (usually)
- outside (ECF): slightly positive
resting membrane potential in most neurons is usually how much
-70 millivolts
membrane is said to be polarized at this stage (resting stage)
concentration values of Na+ & K+ inside & outside the cell
Na+ (outside): 142 mEq/L
Na+ (inside): 14 mEq/L
K+ (outside): 4 mEq/L
K+ (inside): 140 mEq/L
basically Na+ = 14/142 (inside/outside)
K+ = 140/4 (inside/outside)
cell membrane is a lot more permeable to K+ than Na+
factors responsible for the resting membrane potential
-
K+ & Na+ Leak channels: passive channels that are always slightly open
- allow K+ to leak out of call and Na+ to leak in
- keeps the inside more negative -
Na+/K+ ATPase pump: active pump that uses ATP to move:
- 3 Na+ ions out
- 2 K+ ions in
maintains the ion gradients since net charge is staying at negative - K+ & Na+ diffusion potentials
- Impermeant intracellular anions: proteins, sulfates, phosphates that stay inside cell always and are negatively charged- contribute a lil bit to the negativity
equilibrium potential for K+ & Na+
K+: -94 mV
Na+: +61 mV
voltage at which the ion doesn’t wanna move anymore b/c electrical force pulling in = conc. gradient pushing out
equilibrium potential vs diffusion potential (for own knowledge)
equilibrium potential: membrane potential at which one specific ion is in electrochemical balance (no net movement)
- theoretical value
diffusion potential: voltage created by ions moving across the membrane due to concentration gradients
- actual effect caused by ion movement
electrical gradient opposes the ________
concentration (chemical) gradient
what is the assumption of the Nernst potential?
assumption: that the cell membrane is permeable only to that specific ion (can obv only occur in experimental conditions & not in real cells)
Goldman equation (Goldman-Hodgkin-Katz) + what does it calculate the resting membrane potential to be
actual formula that calculates the real membrane potential b/c it takes into account that the membrane is permeable to several different ions
- whereas, Nernst potential assumes that its only permeable to that one
calculates resting membrane potential to be -86 mV then Na+/K+ pump adds -4 mV & then contribution of Ca2+ ions as well - around -90 mV for most muscle cells
why does the resting membrane potential only take into account Na+ & K+ ions? (more or less for own knowledge)
b/c they have:
- active pump
- large concentration gradients
- large permeabilities
lack of these characteristics for other ions just makes their effect negligible
clinical relevance of membrane potentials
basis of all electrical signals in the body, esp muscle & nerves
Electrodiagnostics: ECG, EMG, NCS
1. ECG (electrocardiography): recording of electrical activity of the heart
- depolarization & repolarization generate currents that are picked up electrodes
-
EMG (electromyography): measures electrical activity in skeletal muscles
- helps diagnose muscle or nerve disorders - NCS (nerve conduction studies): measures how fast/strong electrical impulses travel along a nerve
-
Local anesthesia: block nerve signals in a specific area by blocking voltage-gated Na+ channels
- neuron cant depolarize and no action potential so patient doesn’t feel pain!
define action potential
“Brief, Rapid, large and reversible change in resting membrane potential of an excitable cell during which the membrane potential reverses”
- attribute of excitable cells like nerve & muscle cells (whereas resting membrane potential exists in all cells)
- simply the reversal of charge distribution so becomes pos. instead of neg.
what are the ions responsible for action potential?
- sodium (move in to create positivity)
- potassium (move outward to create +)
- calcium
explain the 3 stages of action potential
1. Resting stage: membrane potential is at rest is at -70 mV before any action potential occurs
- ion concentrations are unequal
- membrane said to be “polarized” here
2. Depolarization stage: opening of voltage gated Na+ channels causes Na+ to come into cell
- potential starts to rise rapidly towards positive direction
- potential goes towards 0 and then +35 (for overshoot)
- ONLY HAPPENS AFTER THRESHOLD POTENTIAL CROSSED (-55 mV)
3. Repolarization stage: Na+ channels begin to close and K+ channels begin to open
- re-establishment of normal negative resting potential
+35 to -70
Hyperpolarization: undershoot, becomes a bit more neg. b/c of the K+ channels taking time to close so more K+ coming in than normal
inactivation/activation gates of Na+ ion channels during the different stages of the action potential
controlled by membrane voltage, K+ doesn’t have these 2 gates- it only has 1
- Resting Stage: activation gate closed, inactivation gate opened
-
Depolarization (threshold reached): activation gate opens quickly, inactivation gate is also still open
- Na+ starts to rush in -
Peak of depolarization: inactivation gate closes (delayed), activation gate is still open
- Na stops entering, channel becomes inactive -
Repolarization: inactivation gate reopens slowly, activation gate closes
- back to resting state
how do the inactivation/activation gates of Na+ channel contribute to the refractory period?
When the inactivation gate is closed, no new action potential can happen (at the peak of depolarization)
and inactivating gate will not reopen until membrane potential returns to original resting membrane potential levels
what are graded potentials?
local, short-lived changes in a cell’s membrane potential that vary in strength & duration, depending on the stimulus
- can either be excitatory (depolarizing) or inhibitory (hyper polarizing)
not a true action potential
basically stimulus is coming in constantly, but all of them are not enough to actually generate the action potential
3 types of stimuli for action potential (they all fall under graded potential)
-
Subthreshold stimulus: local changes in membrane potential at which action potential cannot be initiated
- like very light press
- below -55 mV -
Threshold stimulus: local changes in membrane potential at which action potential can be initiated
- normal press
- usually around -55 mV -
Suprathreshold stimulus: local changes at which potential rises above threshold value
- hard press
- beyond -55 mV
opening of ligand or technically gated channels generates ________
graded potential
graded potential can then initiate action potential when it reaches the threshold value
properties of action potential: increasing stimulus strength
Strength of Stimulus Doesn’t Affect Size of Action Potential
due to the “All-or-none” principle - once threshold is reached, you get a full action potential no matter if the stimulus was just enough or very strong (no bigger AP w/ bigger stimulus)
however, increasing stimulus strength won’t increase size of AP but will increase frequency of APs
properties of action potentials: non-decremental propagation
non-decremental conduction: action potentials travel along the axon without losing strength as they go
- AP is regenerated at each segment of the axon by opening Na⁺ channels to not lose magnitude
contrast this with graded potentials, which fade over distance (decremental propagation)
absolute vs relative refractory period
absolute refractory period: neuron CANNOT respond to another stimulus
- time from opening of Na+ activation gates until closing of inactivation gates
relative refractory period: shortly after absolute refractory period, if stimulus is STRONGER than normal, then it can trigger a new AP
- some Na+ gates are closed & ready to reopen but K+ gates are still open and repolarization is occurring
why does a plateau phase occur in the action potential of cardiac muscle (ventricular myocyte) & what is the significance?
Voltage-activated calcium-sodium channels (L-type): are slow to open, prolonged opening of these channels causes Ca²⁺ to flow in slowly
K+ channels: these also take longer to open in cardiac muscle, usually open at the end of the plateau phase
significance:
- allows for prolonged contraction (need to stay contracted long enough to eject blood)
- prevents tetany (sustained contraction if stimuli come too fast, so protects heart from going into continuous contraction which could be fatal)
myelinated vs. unmyelinated nerve fibers
unmyelinated: large fibers, axons without myelin sheath
- SLOWER conduction of impulse
- impulse travels continuously along axon (continuous conduction)
- found in places where speed isn’t critical (ex. autonomic post ganglionic fibers)
myelinated: small fibers, axons wrapped in myelin (which is produced by schwann cells)
- very FAST conduction
- saltatory conduction
- found where speed is essential (ex. motor neurons)
saltatory conduction + 2 benefits UQ
jumping of the action potential from one node of ranvier to the next in a myelinated nerve fiber– instead of continuously traveling along the entire axon
benefits:
1. increases velocity of nerve transmission (imagine throwing b/w people vs passing)
- conserves energy for axon bc only the nodes depolarize so much less energy is used & less ions are used up
4 factors that affect action potential propagation speed in nerve fibers
- axon diameter: large diameter axon has less resistance to current flow = faster AP travels
- myelination: acts as insulator & does saltatory conduction so goes faster
- temperature: higher temps increase rate of ion channel opening = faster propagation
- internode length: distance b/w nodes of ranvier affects speed of saltatory conduction
resting membrane potential in smooth muscle
typically -50 to -60 mV (less negative than skeletal muscle)
2 types of action potentials in single-unit (visceral) smooth muscle
AP mainly drive by Ca2+ rather than Na+ (like in skeletal muscle)
-
Spike potentials: quick, sharp depolarization & repolarization
- occur in most single-unit smooth muscle
- triggered by: electrical stimulation, stretch, neurotransmitters, spontaneous activity -
Action potentials with plateaus: initial depolarization similar to spike potentials, has a stage of delayed depolarization that results in prolonged contraction
- occurs in specialized smooth muscles that need long-lasting contractions (ex. uterus during labor & ureter during urine movement)
slow wave potentials + causes
rhythmic, spontaneous (no nerve input required) oscillations in the resting membrane potential of single-unit (visceral) smooth muscle cells
- switching b/w positive and negative but are still below the threshold potential
only in smooth muscles- look like waves
can trigger action potential but is not the real action potential
causes:
1. rhythmic changes in ion channel activity: special types of ion channels in these cells that open and close on their own - not always voltage dependent (like GI smooth muscles)
- Na+/K+ activity: variations in this opening/closing
spontaneous action potentials & stretch response
spontaneous action potentials: In visceral (single-unit) smooth muscle, muscle cells can fire action potentials on their own, without any nerve signal
When visceral smooth muscle is stretched (like when food enters the gut):
- membrane negativity reduced (stretching physically opens ion channels) = closer to threshold
- slow wave activity enhanced: make them reach threshold more easily = triggers AP = muscle contraction
physiological role: body’s way of doing auto-regulation (no signal from brain needed), helps gut wall resist excessive stretch via contraction
