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• Membrane potential = electrical potential difference across cell membrane
• Measured in millivolts (mV)
• Inside of cell is usually negative relative to outside
• Created by unequal distribution of ions
In most cells at rest:
Resting membrane potential ≈ –70 mV (neurons)
It is not electricity flowing — it is stored electrical energy.
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• Positive charges more abundant outside
• Negative charges more abundant inside
• Membrane acts like a capacitor
• Separation of charge occurs across thin membrane (~7–10 nm)
Small charge difference → significant voltage because membrane is extremely thin.
Intracellular fluid (ICF):
• High K⁺
• Low Na⁺
• High negatively charged proteins
• Low Ca²⁺
Extracellular fluid (ECF):
• High Na⁺
• High Cl⁻
• Low K⁺
• High Ca²⁺
These differences are actively maintained by Na⁺–K⁺ ATPase.
Membrane potential exists because these ionic asymmetries exist.
Excitable tissues:
• Nerve
• Skeletal muscle
• Cardiac muscle
• Smooth muscle
Functions:
• Generation of action potentials
• Nerve impulse conduction
• Muscle contraction
• Synaptic transmission
Without membrane potential, neurons cannot signal and muscles cannot contract.
Electrical polarization is the foundation of excitability.
Resting Potential:
• Stable negative potential in unstimulated cell
• Maintained by:
– K⁺ leak channels
– Na⁺–K⁺ ATPase
– Selective permeability
Action Potential:
• Rapid, transient reversal of membrane potential
• Triggered by opening of voltage-gated channels
• Depolarization → Repolarization → Hyperpolarization
Resting potential is stored energy.
Action potential is rapid discharge of that energy.
• Hyperkalemia → decreased membrane negativity → cardiac arrhythmias
• Hypokalemia → increased membrane negativity → muscle weakness
• Local anesthetics block voltage-gated Na⁺ channels
• Epilepsy involves abnormal neuronal excitability
• Long QT syndrome → ion channel defects
• High concentration inside cell
• Low concentration outside
• Most permeable ion at rest
• Major contributor to resting membrane potential
K⁺ wants to move out down its concentration gradient.
When it leaves, it makes inside negative.
• High concentration outside
• Low concentration inside
• Low permeability at rest
• Major ion in depolarization
Na⁺ wants to move inside both by concentration and electrical attraction.
Opening Na⁺ channels → rapid depolarization.
• High outside
• Lower inside
• Passively distributed in many cells
• Contributes to stabilization of membrane potential
Often follows electrochemical equilibrium.
• Very low intracellular concentration
• High extracellular concentration
• Strong electrochemical gradient inward
• Important in action potentials (cardiac, smooth muscle)
Intracellular Ca²⁺ is tightly regulated because small increases trigger contraction and secretion.
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Inside (ICF):
• High K⁺
• High negatively charged proteins
• Low Na⁺
• Very low Ca²⁺
Outside (ECF):
• High Na⁺
• High Cl⁻
• Low K⁺
• High Ca²⁺
This asymmetry is the foundation of membrane potential.
No unequal distribution → no voltage.
• Membrane is more permeable to K⁺ than Na⁺ at rest
• K⁺ leak channels are abundant
• Na⁺ channels mostly closed at rest
Because K⁺ permeability is high:
Resting membrane potential lies close to K⁺ equilibrium potential.
Membrane potential is determined by permeability, not just concentration.
• Pumps 3 Na⁺ out
• Pumps 2 K⁺ in
• Maintains ionic gradients
• Slightly electrogenic
Primary functions:
• Maintains Na⁺ and K⁺ gradient
• Prevents cell swelling
• Indirectly enables action potential
If pump stops → gradients collapse → membrane potential disappears → cell dies.
• K⁺ leak channels → allow passive K⁺ efflux
• Major determinant of resting potential
• Na⁺ leak channels → minor contribution
Leak channels create steady-state voltage.
Without them, no resting membrane potential would exist.
Each ion is influenced by two forces:
Concentration gradient:
• Drives ion from high → low concentration
Electrical gradient:
• Opposite charges attract
• Like charges repel
For K⁺:
• Concentration gradient → pushes K⁺ out
• Electrical gradient → pulls K⁺ in
Equilibrium occurs when both forces balance.
Membrane potential reflects this balance.
• Ions move from high → low concentration
• Driven by concentration gradient
• Example: K⁺ diffuses outward (high inside → low outside)
Diffusion alone would equalize concentrations — if the membrane allowed it.
• Opposite charges attract
• Like charges repel
• Movement of charged ions alters membrane voltage
As K⁺ diffuses out, inside becomes negative.
That negative charge pulls K⁺ back inward.
• Combined effect of concentration + electrical gradient
• Determines net ion movement
• When both forces balance → no net movement
This balance point defines equilibrium potential.
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• Membrane more permeable to K⁺ than Na⁺ at rest
• Many K⁺ leak channels
• Few Na⁺ channels open
Because K⁺ permeability dominates, RMP lies close to K⁺ equilibrium potential.
• Large negatively charged proteins inside cell
• Cannot cross membrane
• Contribute to negative intracellular charge
These trapped anions enhance internal negativity.
• Potential at which net movement of a specific ion stops
• Occurs when electrical force balances diffusion force
• Unique for each ion
Each ion has its own equilibrium potential.
RMP is not equal to one ion’s equilibrium potential —
it is a weighted average based on permeability.
• Occurs due to impermeant charged proteins inside cell
• Creates unequal distribution of diffusible ions
• Leads to slight osmotic imbalance
The Donnan effect contributes modestly to resting potential and cell swelling tendency.
Now we quantify equilibrium potential.
• Nernst potential = equilibrium potential of a single ion
• Electrical potential that exactly opposes diffusion
At this voltage, net ion movement is zero.
E = (RT / zF) ln ( [Ion outside] / [Ion inside] )
At 37°C, simplified form:
E (mV) ≈ 61 / z × log (outside / inside)
Where:
• z = valency of ion
• R = gas constant
• T = temperature
• F = Faraday constant
If membrane potential equals Nernst potential of an ion:
• No net movement of that ion
• Ion is in electrochemical equilibrium
Example:
If membrane potential = –90 mV (approx K⁺ equilibrium)
→ K⁺ net flux = zero.
• Higher gradient → larger equilibrium potential
• Ratio matters, not absolute concentration
• Change extracellular K⁺ → dramatic change in RMP
Clinical:
Hyperkalemia → RMP becomes less negative → arrhythmias.
• Nernst potential depends on temperature
• Higher temperature → slightly higher equilibrium voltage
• Physiological calculations use 37°C
Thermodynamics always sneaks in.
For K⁺:
Typical values:
Outside ≈ 4 mEq/L
Inside ≈ 140 mEq/L
E_K ≈ –90 mV
For Na⁺:
Outside ≈ 140 mEq/L
Inside ≈ 10–15 mEq/L
E_Na ≈ +60 mV
For Cl⁻:
Outside ≈ 100 mEq/L
Inside ≈ 10–20 mEq/L
E_Cl ≈ –70 mV (approx)
• RMP lies close to K⁺ equilibrium potential
• Because K⁺ permeability is highest at rest
• Small Na⁺ permeability makes RMP slightly less negative than E_K
Thus:
RMP ≈ weighted average of equilibrium potentials
(primarily K⁺, slightly Na⁺ and Cl⁻)
• Mathematical equation used to calculate membrane potential
• Considers multiple ions simultaneously
• Accounts for relative permeability of each ion
Unlike Nernst, which calculates equilibrium potential for a single ion,
GHK calculates the actual membrane potential when several ions contribute.
Nernst equation:
• Works for one ion only
• Assumes membrane permeable only to that ion
Reality:
• Membrane is permeable to K⁺, Na⁺, and Cl⁻ at rest
• Each contributes differently
Therefore, resting membrane potential (RMP) is not equal to EK alone.
GHK gives a more accurate estimate.
GHK includes:
• Potassium (K⁺)
• Sodium (Na⁺)
• Chloride (Cl⁻)
The simplified conceptual form:
Vm depends on:
(PK × [K⁺]out + PNa × [Na⁺]out + PCl × [Cl⁻]in)
divided by
(PK × [K⁺]in + PNa × [Na⁺]in + PCl × [Cl⁻]out)
Important:
• Permeability terms (P) matter greatly
• Chloride is reversed in equation because it is negatively charged
At rest:
PK >> PNa
PK > PCl (varies by cell type)
Because potassium permeability dominates:
• RMP is close to EK (–90 mV)
• But slightly less negative (~ –70 mV in neurons)
Even small sodium permeability shifts RMP toward ENa (+60 mV).
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• Explains why RMP ≠ EK exactly
• Explains how changes in permeability alter membrane potential
• During action potential, PNa increases → Vm moves toward ENa
Membrane potential is dynamic because permeability changes.
• Hyperkalemia → reduced K⁺ gradient → RMP less negative
• Hypokalemia → more negative RMP
• Ischemia → altered permeability → depolarization
• Anesthetics alter ion permeability
GHK helps explain arrhythmias and neuronal excitability disorders.
Now we introduce a quieter but important concept.
• Describes distribution of ions across membrane
• Occurs when membrane is permeable to some ions
• But impermeable to at least one charged species
Typically:
• Large negatively charged proteins inside cell
• Cannot cross membrane
Inside cell:
• Large proteins (A⁻)
• Cannot leave
• Carry negative charge
To maintain electrical neutrality:
• Diffusible cations (e.g., K⁺) accumulate inside
• Some anions distribute unevenly
This is the Donnan effect.
At equilibrium:
• Product of diffusible cations and anions equal on both sides
But distribution is unequal because of trapped anions.
Result:
• Slight electrical potential difference
• Slight osmotic imbalance
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• More osmotically active particles inside cell
• Water tends to enter cell
• Risk of swelling
Na⁺–K⁺ ATPase counters this by pumping Na⁺ out.
Without active transport, cells would swell and rupture.
• Contributes modestly to RMP
• More important in osmotic balance
• Maintains intracellular negativity
But main RMP determinant remains selective permeability to K⁺.
• Hypoproteinemia → edema (plasma Donnan effects)
• Renal failure → altered ionic distribution
• Loss of pump function → cellular swelling
Donnan effect explains why cells need constant active transport to avoid osmotic disaster.
Here is the hierarchy:
Nernst → equilibrium of one ion
GHK → combined influence of multiple ions
Donnan → influence of trapped non-diffusible ions
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• Fine glass microelectrode filled with electrolyte solution
• Tip diameter < 1 µm
• Inserted into cell cytoplasm
• Measures potential difference between inside and outside
One electrode goes inside the cell.
The other stays in extracellular fluid.
The voltage difference between them = membrane potential.
• Electrode penetrates cell membrane
• Direct measurement of membrane potential
• Resting potential seen as negative deflection
Typical neuron RMP ≈ –70 mV.
When electrode enters cell, the trace suddenly drops downward — that drop is biology revealing its charge asymmetry.
• Placed in extracellular fluid
• Provides zero reference point
• Allows measurement of potential difference
Membrane potential is always measured relative to outside.
No reference → no meaningful voltage.
• Electrical signal displayed on screen
• Resting potential → steady negative line
• Action potential → sharp spike
This visual record transforms invisible ion movement into visible electrical events.
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• Developed by Neher and Sakmann
• Glass pipette forms tight seal with membrane
• Can record current from:
– Single ion channel
– Whole cell
Allows measurement of picoampere-level currents.
This technique proved that ion channels open and close in discrete steps.
Electricity at the level of individual proteins.
• Study of ion channel function
• Understanding channelopathies
• Drug testing on ion channels
• Neuroscience research
Without patch-clamp, modern electrophysiology would not exist.
Now we compare local electrical whispers with full electrical explosions.
• Small, local change in membrane potential
• Can be depolarization or hyperpolarization
• Occurs in dendrites and cell body
Usually caused by ligand-gated channel opening.
• Confined to small membrane region
• Does not travel long distances
• Amplitude decreases with distance
• Fades as it spreads
Because current leaks through membrane.
Graded potentials are like ripples in water — strong near the source, weaker farther away.
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• Rapid, transient reversal of membrane potential
• Occurs when threshold is reached
• Generated by voltage-gated channels
• Propagates along axon without decrement
Phases:
• Depolarization (Na⁺ influx)
• Repolarization (K⁺ efflux)
• Hyperpolarization
• Critical membrane potential required to trigger action potential
• Usually around –55 mV in neurons
• Below threshold → no AP
• Above threshold → full AP
Threshold is the decision point.
• Action potential either occurs fully or not at all
• No partial spikes
• Amplitude does not depend on stimulus strength
Stronger stimulus increases frequency, not amplitude.
This binary behavior makes neural signaling reliable.
Graded Potential:
• Variable amplitude
• Local
• Decremental
• No threshold
• Can summate
Action Potential:
• Fixed amplitude
• Propagated
• Non-decremental
• Requires threshold
• All-or-none
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• Membrane potential ≈ –70 mV
• High K⁺ permeability
• Voltage-gated Na⁺ and K⁺ channels closed
• Na⁺–K⁺ ATPase maintains gradients
Cell is polarized and ready.
• Stimulus reaches threshold (~ –55 mV)
• Voltage-gated Na⁺ channels open rapidly
• Massive Na⁺ influx
• Membrane potential becomes less negative
• Overshoot → reaches around +30 to +40 mV
Positive feedback:
More depolarization → more Na⁺ channels open.
• Na⁺ channels inactivate
• Voltage-gated K⁺ channels open
• K⁺ efflux occurs
• Membrane potential returns toward negative
Reversal of polarity begins.
• K⁺ channels remain open slightly longer
• Excess K⁺ leaves cell
• Membrane potential becomes more negative than resting (~ –80 mV)
Eventually K⁺ channels close → RMP restored.
• Minimum membrane potential required to trigger AP
• Usually ~ –55 mV
• Below threshold → no AP
• Above threshold → full AP
Threshold represents the critical number of Na⁺ channels activated.
• Local depolarization spreads to adjacent membrane
• Triggers opening of voltage-gated Na⁺ channels in next segment
• Action potential regenerates along axon
• Non-decremental conduction
Each segment triggers the next — like falling dominoes.
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• Occurs in myelinated fibers
• Myelin acts as electrical insulator
• Action potential jumps from one Node of Ranvier to next
• Faster conduction
• Energy efficient
Multiple sclerosis → demyelination → slowed conduction.
• During depolarization and early repolarization
• No new AP possible
• Na⁺ channels are inactivated
Ensures one-way propagation.
• During hyperpolarization
• Stronger stimulus required
• Some Na⁺ channels recovered
• K⁺ channels still open
Limits firing frequency.
Now we dissect the channel mechanics.
• Have activation gate and inactivation gate
• Open rapidly at threshold
• Responsible for depolarization phase
Structure allows extremely fast response.
• Large electrochemical gradient inward
• Drives membrane potential toward ENa (+60 mV)
• Responsible for overshoot
Depolarization is sodium’s moment of dominance.
• Close shortly after channel opens
• Stop Na⁺ influx
• Responsible for absolute refractory period
Even if stimulus continues, inactivated channels cannot reopen immediately.
• Voltage-gated K⁺ channels open more slowly
• Activated during depolarization
• Responsible for repolarization
They are delayed rectifiers.
• K⁺ leaves cell down concentration gradient
• Restores negativity
• Causes hyperpolarization when excessive
Potassium restores order.
• K⁺ channels close
• Na⁺ channels reset (activation closed, inactivation open)
• Na⁺–K⁺ ATPase maintains gradients
Pump does not directly repolarize —
it maintains long-term ionic gradients.
• Na⁺ channels inactivated
• Cannot reopen until membrane repolarizes
• No second AP possible
Prevents backward conduction.
• Some Na⁺ channels recovered
• K⁺ permeability still high
• Membrane hyperpolarized
• Stronger stimulus required
Determines maximum firing frequency.
• Much longer duration (≈ 200–300 ms in ventricle)
• Prominent plateau phase
• Calcium plays major role
• Prevents tetany
• Refractory period nearly equals contraction time
Neurons spike briefly.
Cardiac cells hold the voltage longer — to ensure rhythmic contraction.
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• Opening of fast voltage-gated Na⁺ channels
• Rapid Na⁺ influx
• Membrane potential rises to about +20 mV
Similar to nerve depolarization.
• Na⁺ channels inactivate
• Transient outward K⁺ current
• Slight fall in membrane potential
Short-lived phase.
• Opening of L-type Ca²⁺ channels
• Ca²⁺ influx
• Balanced by K⁺ efflux
• Membrane potential remains near 0 mV
This plateau prolongs depolarization.
Calcium entry here triggers contraction (excitation–contraction coupling).
• Ca²⁺ channels close
• Increased K⁺ efflux
• Membrane potential returns to resting
Dominated by potassium currents.
• Stable resting potential (~ –90 mV in ventricles)
• Maintained by K⁺ permeability
• Na⁺–K⁺ ATPase maintains gradients
• L-type Ca²⁺ channels open in Phase 2
• Responsible for plateau
• Trigger Ca²⁺ release from sarcoplasmic reticulum
• Essential for contraction
Without Ca²⁺ influx → no coordinated ventricular contraction.
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Seen in SA node:
• No stable resting potential
• Slow spontaneous depolarization (Phase 4)
• Due to “funny” current (If) and Ca²⁺ influx
• Generates rhythmic heartbeat
Heart does not wait for external command.
It is self-exciting.
Antiarrhythmic drugs target ion channels:
Class I → Block Na⁺ channels
Class II → Beta blockers (reduce sympathetic input)
Class III → Block K⁺ channels (prolong repolarization)
Class IV → Block Ca²⁺ channels
Understanding phases = understanding drug mechanism.
Long QT syndrome → prolonged Phase 3 → arrhythmia risk.
• If threshold reached → full action potential
• If not → none
• Amplitude independent of stimulus strength
Stronger stimulus increases frequency, not amplitude.
• Na⁺ channels inactivated
• No second AP possible
• Ensures unidirectional conduction
In heart, very long → prevents tetany.
• Some Na⁺ channels recovered
• Stronger stimulus required
• Occurs during late repolarization
Determines maximum firing rate.
• Gradually rising stimulus may fail to trigger AP
• Because Na⁺ channels inactivate slowly
• Threshold shifts
Seen in nerve excitability testing.
• Speed of action potential propagation
• Depends on:
– Axon diameter
– Myelination
– Temperature
Large, myelinated fibers conduct fastest.
• Fiber diameter
• Myelination
• Membrane resistance
• Internal resistance
• Electrolyte disturbances
• Drugs (local anesthetics)
Hyperkalemia → decreased excitability
Hypokalemia → delayed repolarization
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• Open in response to change in membrane potential
• Essential for action potentials
• Found in nerve, skeletal muscle, cardiac muscle
Examples:
• Na⁺ channels → depolarization
• K⁺ channels → repolarization
• Ca²⁺ channels → plateau (heart)
Contain voltage-sensing domain (S4 segment with positive charges).
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• Open when specific chemical binds
• Found at synapses
• Fast synaptic transmission
Examples:
• Nicotinic acetylcholine receptor
• GABA-A receptor (Cl⁻ channel)
Convert chemical signal into electrical change.
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• Open in response to stretch or pressure
• Present in:
– Touch receptors
– Baroreceptors
– Inner ear hair cells
Convert physical force into electrical signal.
General features:
• Transmembrane protein
• Multiple α-helical segments
• Central aqueous pore
• Selectivity filter
• Activation and inactivation gates
Selectivity filter ensures:
• K⁺ channel passes K⁺ but not Na⁺
• Based on size and hydration energy
Structure determines specificity.
Three major mechanisms:
Voltage gating:
• Responds to membrane potential changes
Ligand gating:
• Responds to neurotransmitter binding
Mechanical gating:
• Responds to membrane deformation
Channels can exist in three states:
• Closed
• Open
• Inactivated
Inactivation prevents continuous ion flow.
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Developed by Neher and Sakmann.
• Glass micropipette seals onto membrane
• Records ionic currents
• Can measure single-channel activity
• Modes:
– Cell-attached
– Whole-cell
– Inside-out
– Outside-out
Revealed that ion channels open in discrete steps — not gradually.
Electrical activity at picoampere level.
Diseases caused by ion channel dysfunction.
Examples:
• Cystic fibrosis → defective CFTR (Cl⁻ channel)
• Long QT syndrome → K⁺ channel mutation
• Epilepsy → Na⁺ or Ca²⁺ channel abnormalities
• Myasthenia gravis → ACh receptor defect
• Periodic paralysis → Na⁺ channel mutation
Small molecular defect → large physiological disturbance.
• Local anesthetics block voltage-gated Na⁺ channels
• Antiarrhythmics modify cardiac ion channels
• Benzodiazepines enhance GABA-A receptor function
• Calcium channel blockers treat hypertension
Modern pharmacology is largely ion channel modulation.
• Electrical potential difference across cell membrane
• Due to unequal distribution of ions
• Inside usually negative relative to outside
• High K⁺ permeability at rest
• K⁺ diffuses out → leaves behind negative proteins
• Slight Na⁺ permeability modifies it
• Na⁺–K⁺ ATPase maintains gradients
RMP ≈ –70 mV (neurons), ≈ –90 mV (ventricular muscle).
• Potassium (K⁺)
Because membrane is most permeable to K⁺ at rest.
• Membrane potential at which net movement of a specific ion stops
• Calculated using Nernst equation
• Membrane also slightly permeable to Na⁺ and Cl⁻
• Goldman-Hodgkin-Katz equation considers multiple ions
• Decreased K⁺ gradient
• RMP becomes less negative
• Increased excitability initially
• Risk of cardiac arrhythmia
• Critical membrane potential required to trigger action potential
• Usually ~ –55 mV in neurons
Below threshold → no AP.
Above threshold → full AP.
• Action potential either occurs completely or not at all
• Amplitude independent of stimulus strength
• Stronger stimulus increases frequency, not size
• It is regenerated at each segment
• Voltage-gated Na⁺ channels open sequentially
• Non-decremental conduction
• Rapid opening of voltage-gated Na⁺ channels
• Na⁺ influx
• Inactivation of Na⁺ channels
• Opening of voltage-gated K⁺ channels
• K⁺ efflux
• K⁺ channels remain open longer
• Excess K⁺ efflux
• Period when Na⁺ channels are inactivated
• No second AP possible
Ensures one-way conduction.
• Occurs during hyperpolarization
• Stronger stimulus required
• Some Na⁺ channels recovered
• Presence of plateau phase
• L-type Ca²⁺ channel activity
• Prevents tetany
• AP jumps from one node of Ranvier to next
• Occurs in myelinated fibers
• Faster and energy-efficient
• Spontaneous slow depolarization in SA node
• Due to funny current (If) and Ca²⁺ influx
• Generates rhythmic heartbeat
• Gradually increasing stimulus may fail to trigger AP
• Due to slow Na⁺ channel inactivation
• Axon diameter
• Myelination
• Membrane resistance
• Temperature
Large, myelinated fibers conduct fastest.
• Calculates membrane potential considering multiple ions
• More accurate than Nernst for RMP
• Caused by impermeant intracellular proteins
• Alters distribution of permeable ions
• Creates slight osmotic imbalance
• Class I → block Na⁺ channels
• Class III → block K⁺ channels
• Class IV → block Ca²⁺ channels
Target specific phases of cardiac AP.
• It maintains ionic gradients
• Does not produce rapid voltage change
• Supports long-term membrane potential stability
• High intracellular Ca²⁺ triggers contraction and secretion
• Regulated by Ca²⁺ ATPase and Na⁺–Ca²⁺ exchanger
A. Sodium
B. Calcium
C. Potassium
D. Chloride
Answer: C
A. –30 mV
B. –55 mV
C. –70 mV
D. +60 mV
Answer: C
A. Goldman equation
B. Nernst equation
C. Fick’s law
D. Van’t Hoff equation
Answer: B
A. Ignores ion permeability
B. Applies only to potassium
C. Considers multiple ions and their permeability
D. Calculates osmotic pressure
Answer: C
A. K⁺ influx
B. Na⁺ efflux
C. Na⁺ influx
D. Cl⁻ influx
Answer: C
A. Opening of K⁺ channels
B. Inactivation of Na⁺ channels
C. Closure of K⁺ channels
D. Activation of Cl⁻ channels
Answer: B
A. Excess Na⁺ entry
B. Delayed closure of K⁺ channels
C. Ca²⁺ influx
D. Cl⁻ exit
Answer: B
A. –90 mV
B. –70 mV
C. –55 mV
D. +30 mV
Answer: C
A. AP amplitude depends on stimulus strength
B. AP amplitude is constant once threshold is reached
C. Subthreshold stimulus produces small AP
D. AP gradually increases in size
Answer: B
A. Unmyelinated fibers only
B. Cardiac muscle
C. Myelinated nerve fibers
D. Smooth muscle
Answer: C
A. Rapid Na⁺ influx
B. Persistent K⁺ efflux
C. L-type Ca²⁺ channel opening
D. Cl⁻ influx
Answer: C
A. More negative
B. Less negative
C. Unchanged
D. Equal to ENa
Answer: B
A. Rapid Na⁺ channels
B. Funny current (If) and Ca²⁺ influx
C. Cl⁻ channels
D. K⁺ leak channels only
Answer: B
A. Ion concentration
B. Axon diameter
C. Glucose level
D. Protein synthesis
Answer: B
A. +60 mV
B. –90 mV
C. –55 mV
D. 0 mV
Answer: B
A. All Na⁺ channels are inactivated
B. Membrane is depolarized above threshold
C. Membrane is hyperpolarized and some Na⁺ channels recovered
D. K⁺ channels are closed
Answer: C
A. Increased Na⁺ leak
B. Blockade of Ca²⁺ channels
C. Blockade of K⁺ channels
D. Increased Cl⁻ conductance
Answer: C
A. Voltage-gated channels
B. Impermeant intracellular proteins
C. Na⁺–K⁺ pump failure
D. Increased temperature
Answer: B
A. EK
B. ENa
C. ECl
D. RMP
Answer: B
A. K⁺ channels
B. Ca²⁺ channels
C. Voltage-gated Na⁺ channels
D. Cl⁻ channels
Answer: C
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