review questions:
1. what are the pre-conditions for the formation of resting potential?
2. how does resting potential form?
3. please elucidate the mechanism of action potential formation.
4. what is n-m junction and how does it work?
5. please explain the whole process of muscle contraction?

Question

review questions:
1. what are the pre-conditions for the  formation of resting potential?
2. how does resting potential form?
3. please elucidate the mechanism of action potential formation.
4. what is n-m junction and how does it work?
5. please explain the whole process of muscle contraction?

Accepted Answer

### Question 1
# Brief Explanations:
The pre - conditions for the formation of resting potential mainly include: 1. The cell membrane has different permeability to different ions. The cell membrane is much more permeable to $K^+$ than to $Na^+$ at rest. 2. There is a concentration gradient of ions inside and outside the cell. For example, the concentration of $K^+$ inside the cell is much higher than that outside the cell, while the concentration of $Na^+$ outside the cell is much higher than that inside the cell. This ion concentration gradient is mainly maintained by the sodium - potassium pump ($Na^+/K^+$ - ATPase), which continuously transports 3 $Na^+$ out of the cell and 2 $K^+$ into the cell, consuming ATP.
# Answer:
The pre - conditions for resting potential formation are: 1. The cell membrane has selective permeability to ions (higher permeability to $K^+$ at rest). 2. There is an ion concentration gradient inside and outside the cell (high $K^+$ inside, high $Na^+$ outside), maintained by the sodium - potassium pump.

### Question 2
# Brief Explanations:
At rest, due to the high permeability of the cell membrane to $K^+$, $K^+$ flows out of the cell along its concentration gradient. As $K^+$ flows out, positive charges are carried out of the cell, making the inside of the cell negatively charged and the outside positively charged. When the electrical potential difference generated by the outward flow of $K^+$ (which tends to pull $K^+$ back into the cell) is equal in magnitude and opposite in direction to the concentration gradient - driven outward flow of $K^+$, the net flow of $K^+$ stops. At this time, the potential difference across the cell membrane is the resting potential (about - 70mV in neurons), and the cell is in a polarized state.
# Answer:
Resting potential forms as follows: $K^+$ flows out of the cell along its concentration gradient (due to the high permeability of the cell membrane to $K^+$ at rest). The outward flow of $K^+$ creates a potential difference (inside negative, outside positive) that counteracts the concentration - driven $K^+$ outflow. When the two forces (concentration gradient and electrical potential difference) are balanced, the net $K^+$ flow stops, and the potential difference at this time is the resting potential.

### Question 3
# Brief Explanations:
1. Depolarization phase: When a stimulus reaches the threshold, the cell membrane's permeability to $Na^+$ suddenly increases. $Na^+$ flows into the cell along its concentration gradient and electrical gradient (the inside of the cell is negative at rest, which attracts $Na^+$). The influx of $Na^+$ makes the inside of the cell positively charged, and the membrane potential reverses (from - 70mV to about + 30mV), this is depolarization.
2. Repolarization phase: After depolarization, the permeability of the cell membrane to $Na^+$ rapidly decreases, while the permeability to $K^+$ increases. $K^+$ flows out of the cell along its concentration gradient (high $K^+$ inside) and electrical gradient (inside positive at this time, which repels $K^+$), making the membrane potential return to the resting potential level, this is repolarization.
3. Hyperpolarization phase (sometimes occurs): Due to the relatively slow inactivation of $K^+$ channels, $K^+$ may continue to flow out for a short time, making the membrane potential more negative than the resting potential (e.g., - 90mV), and then return to the resting potential. The sodium - potassium pump then restores the ion concentration gradient to the resting state.
# Answer:
The mechanism of action potential formation:
1. Depolarization: Threshold stimulus causes $Na^+$ channels to open, $Na^+$ influx, membrane potential reverses (depolarization).
2. Repolarization: $Na^+$ channels inactivate, $K^+$ channels open, $K^+$ efflux, membrane potential returns to resting level.
3. (Optional) Hyperpolarization: $K^+$ channels inactivate slowly, $K^+$ continues to efflux briefly, then the sodium - potassium pump restores ion gradients.

### Question 4
# Brief Explanations:
The N - M junction (neuromuscular junction) is the synapse between a motor neuron and a skeletal muscle fiber. Its structure includes the presynaptic membrane (the axon terminal membrane of the motor neuron), the synaptic cleft (the gap between the presynaptic membrane and the postsynaptic membrane), and the postsynaptic membrane (the motor end - plate of the muscle fiber, with a large number of acetylcholine (ACh) receptors).
The working process: 1. The action potential of the motor neuron reaches the axon terminal, causing voltage - gated $Ca^{2+}$ channels to open. $Ca^{2+}$ flows into the axon terminal, triggering the release of ACh from synaptic vesicles into the synaptic cleft by exocytosis. 2. ACh diffuses across the synaptic cleft and binds to ACh receptors on the motor end - plate, causing the ion channels of the receptors to open. Mainly $Na^+$ and $K^+$ flow through, with a net influx of $Na^+$, leading to depolarization of the motor end - plate, which is called the end - plate potential (EPP). 3. The EPP spreads to the surrounding muscle cell membrane, triggering an action potential in the muscle cell. 4. After ACh exerts its effect, it is quickly hydrolyzed by acetylcholinesterase (AChE) in the synaptic cleft into acetic acid and choline, terminating the signal transmission.
# Answer:
The N - M junction (neuromuscular junction) is the synapse between a motor neuron and a skeletal muscle fiber, consisting of the presynaptic membrane, synaptic cleft, and postsynaptic membrane (motor end - plate). Its working process: 1. Motor neuron action potential causes $Ca^{2+}$ influx at the axon terminal, triggering ACh release. 2. ACh binds to receptors on the motor end - plate, causing end - plate potential (EPP) by ion channel opening. 3. EPP triggers muscle cell action potential. 4. ACh is hydrolyzed by AChE to terminate the signal.

### Question 5
# Brief Explanations:
1. Excitation - contraction coupling: The action potential of the muscle cell spreads along the sarcolemma and into the T - tubules. The change in membrane potential in the T - tubules causes the ryanodine receptors (RyR) on the sarcoplasmic reticulum (SR) to open, releasing $Ca^{2+}$ from the SR into the sarcoplasm.
2. Cross - bridge cycling:
    - Binding: The released $Ca^{2+}$ binds to troponin C (TnC) in the thin filament (composed of actin, troponin, and tropomyosin). This binding causes a conformational change in troponin, which in turn pulls tropomyosin away from the myosin - binding sites on actin. Myosin heads (from the thick filament, composed of myosin) bind to the exposed binding sites on actin, forming cross - bridges.
    - Power stroke: The myosin head, after binding to actin, undergoes a conformational change (power stroke), pulling the thin filament towards the center of the sarcomere (M - line). At this time, ADP and inorganic phosphate (Pi) are released from the myosin head.
    - Detachment: ATP binds to the myosin head, causing the myosin head to detach from actin.
    - Re - energization: ATP is hydrolyzed by myosin ATPase on the myosin head, re - energizing the myosin head and preparing it for the next cycle.
3. Relaxation: When the action potential ends, $Ca^{2+}$ is actively transported back into the SR by the $Ca^{2+}$ - ATPase on the SR membrane. As the $Ca^{2+}$ concentration in the sarcoplasm decreases, $Ca^{2+}$ dissociates from TnC. Troponin - tropomyosin complex returns to its original position, covering the myosin - binding sites on actin. Cross - bridges can no longer be formed, and the muscle relaxes.
# Answer:
The process of muscle contraction:
1. Excitation - contraction coupling: Muscle action potential spreads to T - tubules, triggering $Ca^{2+}$ release from the sarcoplasmic reticulum (SR) into the sarcoplasm.
2. Cross - bridge cycling:
    - Binding: $Ca^{2+}$ binds to TnC, tropomyosin moves, myosin heads bind to actin.
    - Power stroke: Myosin head undergoes power stroke, thin filament moves towards the M - line (ADP and Pi are released).
    - Detachment: ATP binds to myosin head, myosin detaches from actin.
    - Re - energization: ATP is hydrolyzed, myosin head is re - energized.
3. Relaxation: $Ca^{2+}$ is pumped back into SR, $Ca^{2+}$ dissociates from TnC, troponin - tropomyosin covers actin - myosin binding sites, and muscle relaxes.

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