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When the neuron is at rest what does sodium want to do?


When a neuron is at rest, the concentrations of sodium (Na+) and potassium (K+) ions inside and outside the cell are maintained by the sodium-potassium pump in the cell membrane. The sodium-potassium pump uses ATP energy to actively transport 3 Na+ ions out of the cell for every 2 K+ ions pumped in. This establishes concentration gradients with high Na+ outside the cell and high K+ inside. These concentration gradients are critical for generating the action potential when the neuron is stimulated.

Sodium ions want to diffuse down their concentration gradient into the cell when the neuron is at rest. However, the cell membrane is impermeable to Na+ at resting potential due to closed sodium channels. Only the sodium-potassium pump is actively moving Na+ ions out of the cell. When the neuron is stimulated by neurotransmitters binding to receptors on the dendrites, this opens sodium channels in the cell membrane, allowing Na+ to rapidly diffuse into the cell down its concentration gradient. This influx of positive charge from Na+ ions leads to depolarization of the membrane potential, initiating the action potential.

The Role of Ion Concentration Gradients in Neurons

Neurons maintain specific concentration gradients of Na+ and K+ ions across the cell membrane. This gradient is crucial for generating electrical signals in neurons. Here are some key points about the ion gradients:

– Intracellular K+ concentration is high (~400 mM) compared to extracellular K+ (~20 mM)

– Extracellular Na+ concentration is high (~425 mM) compared to intracellular Na+ (~50 mM)

– The sodium-potassium pump uses ATP to pump 3 Na+ out of the cell for every 2 K+ pumped in

– This pump maintains the Na+ and K+ concentration gradients

– At rest, the cell membrane is much more permeable to K+ than Na+ due to closed Na+ channels

– K+ leakage channels allow some K+ to diffuse out down its concentration gradient

– This leads to a negative resting membrane potential of -70 mV, the equilibrium potential for K+

– When Na+ channels open during an action potential, Na+ rushes into the cell down its concentration gradient

– This Na+ influx causes membrane depolarization, initiating the action potential

Therefore, the ion concentration gradients created by the sodium-potassium pump provide the driving force for Na+ entry and membrane depolarization when the neuron becomes activated. Maintaining these Na+ and K+ gradients requires a lot of energy from ATP hydrolysis.

Concentration Gradient Visualization

Ion Extracellular Concentration Intracellular Concentration
Na+ ~425 mM ~50 mM
K+ ~20 mM ~400 mM

This table summarizes the key differences in Na+ and K+ concentrations across the neuronal cell membrane that are critical for electrical signaling.

Sodium Channel Dynamics in the Neuron

When considering what sodium wants to do when the neuron is at rest, it is important to understand the behavior of sodium channels:

– Sodium channels are closed at the resting membrane potential of -70 mV

– Only a small fraction of sodium channels (~1%) are open at rest

– Sodium channels have activation gates that open in response to membrane depolarization

– They also have inactivation gates that close the channel after opening

– When the neuron is stimulated and the membrane depolarizes, the activation gates open rapidly allowing Na+ influx

– Na+ influx causes further depolarization, opening more channels – this positive feedback amplifies the signal

– After a millisecond or so, the inactivation gates close the channels

– During repolarization, a fourth type of channel gate closes the channels and resets their conformation

Therefore, even though the driving force for sodium is strong due to its concentration gradient, the closed state of sodium channels at resting potential prevents any significant Na+ influx. Sodium influx only occurs transiently during the action potential when the channels briefly open before shutting again.

Sodium Channel States

Channel State Description
Closed At resting potential, activation gates are closed
Open Depolarization opens activation gates allowing Na+ influx
Inactivated After opening, inactivation gates close channel pore
Refractory Channel resets its conformation after inactivating

This table summarizes the key conformational states of voltage-gated sodium channels and their behavior during membrane potential changes.

Sodium Ion Movement at Resting Potential

Although the concentration gradient provides a strong driving force for sodium ion influx into the neuron at rest, very little Na+ actually flows into the cell. Here are some key points about sodium ion movement at resting potential:

– The cell membrane is highly impermeable to Na+ when the channels are closed

– Only ~1% of Na+ channels are open, not enough for significant influx

– The sodium-potassium pump actively transports Na+ out of the cell against its gradient

– This maintains the low intracellular Na+ concentration critical for signaling

– Na+ leakage into the cell is minimized due to the closed channels

– Most Na+ movement at rest is via the sodium-potassium pump, not leakage

– When Na+ channels open during depolarization, Na+ rapidly flows down its gradient into the cell

– But this only lasts 1-2 milliseconds before the channels inactivate

– So at rest, sodium cannot effectively permeate the membrane despite its concentration gradient

– The channels must open first to allow rapid influx critical for the action potential

Therefore, the selective permeability of the cell membrane due to the closed sodium channels prevents significant Na+ influx at rest. The sodium-potassium pump maintains the Na+ gradient even with some leakage through open K+ channels.

Sodium Ion Movement at Rest

Condition Na+ Movement
Channels closed Minimal – impermeable to Na+
Pump active Actively transported out of cell
Leakage Some influx through open channels
Balance Pump outpaces leakage to maintain gradient

This table summarizes the key factors affecting sodium ion movement across the neuronal membrane at resting potential.

Sodium Influx During the Action Potential

When the neuron is stimulated and voltage-gated Na+ channels open, Na+ rapidly flows into the cell down its concentration gradient leading to the depolarizing phase of the action potential:

– Stimulus from neurotransmitters causes localized depolarization of the membrane

– This depolarization activates adjacent voltage-gated Na+ channels

– Activation gates open, allowing influx of Na+ ions down the electrochemical gradient

– The Na+ influx causes further depolarization, activating more channels

– This positive feedback loop leads to rapid depolarization as Na+ floods into the cell

– The membrane potential reaches +40 mV at the peak of the action potential

– After 1-2 ms, inactivation gates close the channels

– Na+ influx stops, and K+ efflux repolarizes the membrane

– Na+/K+ pumps restore the ion gradients

– The neuron returns to the resting membrane potential

Therefore, when the sodium channels open transiently during membrane depolarization, sodium is finally able to diffuse rapidly into the cell down its concentration gradient, initiating the action potential. This transient influx underlies neuronal signaling.

Sodium Influx During Action Potential

Stage Description
Resting Channels closed, minimal Na+ influx
Depolarization Channels open, Na+ rushes into cell
Peak Maximum Na+ influx
Inactivation Gates close, Na+ influx stops
Repolarization Efflux of K+ restores resting potential

This table shows the sequence of Na+ channel activation and inactivation underlying the rapid, transient sodium influx during the neuronal action potential.

Conclusion

In summary, even though sodium ions want to enter the neuron down their concentration gradient when the cell is at rest, the closed conformation of voltage-gated sodium channels prevents significant influx of Na+. The sodium-potassium pump maintains the Na+ gradient by actively transporting sodium out of the cell. Only during the brief millisecond timescale when the sodium channels open in response to membrane depolarization can Na+ rapidly diffuse into the neuron, initiating the action potential. Therefore, the selective permeability conferred by sodium channel states allows the neuron to maintain resting membrane potential yet still generate electrical signals through transient sodium influx when stimulated. Understanding these sodium channel dynamics provides key insights into neuronal excitation and communication through action potentials.