nervous system (pt. 2) Flashcards

1
Q

Q: What is the role of action potentials in the body?

A

A: They facilitate both electrical and chemical signals, enabling movement and response to stimuli.

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2
Q

Q: How do action potentials enable communication between neurons and muscle fibers?

A

A: They trigger the release of neurotransmitters at neuromuscular junctions, initiating muscle action potentials.

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3
Q

Q: What structure of the neuron is responsible for transmitting action potentials?

A

A: The axon, which is the long, thread-like part of the neuron.

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4
Q

Q: What happens at the axon terminals during neural communication with muscle fibers?

A

A: Action potentials trigger the release of neurotransmitters into the synaptic gap.

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5
Q

Q: What is the significance of neurotransmitters in muscle fiber activation?

A

A: They cross the synaptic gap and bind to receptors on the muscle fiber, initiating a muscle action potential.

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6
Q

Q: How does a muscle action potential lead to muscle movement?

A

A: It spreads along the surface of the muscle fiber, resulting in muscle contraction.

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7
Q

Q: What ensures that muscle contractions are coordinated and timely?

A

A: The precise control by the nervous system through well-coordinated electrical and chemical changes.

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8
Q

Q: Why are action potentials described as well-coordinated changes?

A

A: They involve sequential electrical changes in neurons that communicate effectively and trigger chemical signals that stimulate muscle fibers.

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9
Q

Q: What is the resting membrane potential in neurons?

A

A: Typically around -70 mV, with the interior more negative than the exterior.

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10
Q

Q: How are ion concentrations distributed at rest?

A

A: K+ is more concentrated inside the neuron; Na+ is more concentrated outside.

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11
Q

Q: What is the role of the sodium-potassium pump?

A

A: It actively transports K+ into the neuron and Na+ out, maintaining concentration differences.

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12
Q

Q: What happens during depolarization?

A

A: Voltage-gated Na+ channels open, allowing Na+ to rush in, making the inside more positive.

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13
Q

Q: How does repolarization occur?

A

A: Voltage-gated K+ channels open, allowing K+ to flow out, restoring the negative membrane potential.

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14
Q

Q: What triggers neurotransmitter release at the neuromuscular junction?

A

A: An action potential reaching the axon terminal.

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15
Q

Q: What happens when neurotransmitters bind to muscle fiber receptors?

A

A: Sodium channels in the muscle membrane open, leading to muscle contraction.

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16
Q

Q: What is the sequence of events in an action potential?

A

A:
1. Stimulus reaches threshold
2. Na+ channels open (depolarization)
3. K+ channels open (repolarization)
4. Return to resting potential

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17
Q

Q: What neurotransmitter is released at the neuromuscular junction?

A

Acetylcholine

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18
Q

Q: What causes the resting membrane potential?

A

A: A buildup of negative ions inside the cell and positive ions outside, creating a charge difference.

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19
Q

Q: What ions are primarily found in extracellular fluid?

A

A: High concentrations of sodium (Na+) and chloride (Cl−).

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20
Q

Q: What ions are primarily found in the cytosol of neurons?

A

A: High concentrations of potassium (K+) and negative ions (like phosphates).

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21
Q

Q: How do K+ channels contribute to resting membrane potential?

A

A: There are more K+ channels than Na+ channels, allowing K+ to leak out, making the inside of the cell more negative.

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22
Q

Q: Why can’t most negative ions inside the cell leave?

A

A: They are attached to larger molecules (like proteins), which helps to maintain the negative charge.

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23
Q

Q: What is the role of the Na+/K+ ATPase pump?

A

A: It actively transports three Na+ ions out of the neuron and two K+ ions into the neuron, maintaining the resting membrane potential.

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24
Q

Q: How does the Na+/K+ pump contribute to the resting membrane potential?

A

A: By moving more Na+ out than K+ in, it helps maintain a negative charge inside the neuron.

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25
Q

Q: What effect does the Na+/K+ pump have on the neuron’s negativity?

A

A: Its activity contributes about -3 mV of the total resting potential of -70 mV.

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26
Q

Q: What happens during depolarization when a neuron is stimulated?

A

A: Sodium channels open, allowing Na+ to enter the neuron, moving the charge closer to the action potential threshold.

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27
Q

Q: What is the importance of the Na+/K+ pump after an action potential?

A

A: It restores the resting potential by removing excess Na+ and bringing K+ back into the neuron.

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28
Q

Q: What are the four types of ion channels?

A

A:
1. Leak channels
2. Ligand-gated channels
3. Mechanically gated channels 4. Voltage-gated channels

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29
Q

Q: What are the characteristics of leak channels?

A

A:
- Open and close randomly
- More K+ channels than Na+ channels
- Found in all cells

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30
Q

Q: What triggers ligand-gated channels?

A

A: Chemical signals like neurotransmitters or hormones.

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31
Q

Q: What activates mechanically gated channels?

A

A: Physical forces like touch, pressure, or stretching.

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32
Q

Q: What is the critical threshold for an action potential?

A

A: -55 millivolts.

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33
Q

Q: How does the Na+/K+ pump maintain ion gradients?

A

A: It moves 3 Na+ out for every 2 K+ in, using ATP for energy.

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34
Q

Q: Describe the charge distribution across the membrane:

A

A: Outside: More positive, high Na+, lower K+ Inside: More negative, high K+, lower Na+, negative proteins

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35
Q

Q: What drives sodium rush during an action potential?

A

A: The electrochemical gradient (concentration difference and electrical attraction).

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36
Q

Q: How do leaky K+ channels affect membrane potential?

A

A: They allow continuous K+ outflow, creating a negative interior (-70mV).

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37
Q

Q: What is the purpose of this ion channel system?

A

A: To ensure:

Stable resting potential
Ready for action potentials
Consistent cellular function
Proper neural signaling

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38
Q

Q: What creates an electrochemical gradient?

A

A: The combination of:

Concentration gradient (ion concentration differences)
Electrical gradient (charge differences across membrane)

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39
Q

Q: What is the resting membrane potential?

A

A: The electrical charge difference (-70 mV) across a neuron’s membrane when not sending signals.

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40
Q

Q: What are the main phases of an action potential?

A

A: 1. Depolarizing phase 2. Repolarizing phase 3. After-hyperpolarizing phase

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41
Q

Q: How do Na+ ions behave in neurons?

A

A: - Higher concentration outside cell

Flow inward when channels open
Attracted by negative internal charge

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42
Q

Q: How do K+ ions behave in neurons?

A

A: - Higher concentration inside cell

Tend to move outward
Movement limited by internal negative proteins

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43
Q

Q: What is the threshold for an action potential?

A

A: -55 mV; depolarization must reach this level to trigger an action potential.

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44
Q

Q: What is the “all-or-none” principle?

A

A: Action potentials occur at full strength or not at all, regardless of stimulus strength.

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45
Q

Q: How do stronger stimuli affect nerve impulses?

A

A: They increase frequency of action potentials, not their intensity.

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46
Q

Q: What happens during depolarization?

A

A: Membrane potential becomes less negative, reaches zero, then becomes positive due to Na+ influx.

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47
Q

Q: What happens during repolarization?

A

A: Membrane potential returns to -70 mV as K+ channels open and K+ flows out.

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48
Q

Q: What membrane potential triggers an action potential?

A

A: -55 mV (threshold potential)

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49
Q

Q: What is the sequence of events after reaching threshold?

A

A: 1. Voltage-gated Na+ channels open 2. Rapid Na+ influx 3. Depolarization begins 4. Positive feedback loop 5. Action potential generation

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50
Q

Q: What is the peak voltage typically reached during an action potential?

A

A: Around +30 mV

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51
Q

Q: What is the positive feedback loop in action potential generation?

A

A: Na+ influx causes more voltage-gated Na+ channels to open, leading to further depolarization.

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52
Q

Q: How does repolarization begin?

A

A: Na+ channels close and voltage-gated K+ channels open.

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53
Q

Q: What is the purpose of depolarization?

A

A: To generate an action potential that can propagate along the axon.

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54
Q

Q: What drives the rapid change in membrane potential?

A

A: The sudden influx of Na+ ions through voltage-gated channels.

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55
Q

Q: What happens to the membrane potential during depolarization?

A

A: It becomes less negative and moves toward positive values.

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56
Q

Q: How does an action potential propagate along an axon?

A

A: It moves as a wave of depolarization, with voltage-gated Na⁺ channels opening sequentially to allow Na⁺ influx.

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57
Q

Q: What is the role of leaky K⁺ channels?

A

A: They allow K⁺ to continuously leak out of the axon, helping maintain the resting membrane potential.

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58
Q

Q: What triggers voltage-gated channels to open?

A

A: Changes in membrane potential (voltage).

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59
Q

Q: How many gates does each voltage-gated Na+ channel have?

A

A: Two gates: an activation gate and an inactivation gate.

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60
Q

Q: What is the state of Na+ channel gates at rest?

A

A: Inactivation gate is open, activation gate is closed, preventing Na+ entry.

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61
Q

Q: What happens to Na+ channel gates at threshold?

A

A: Both activation and inactivation gates open, allowing Na+ inflow.

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62
Q

Q: Why are voltage-gated channels important?

A

A: They participate in the generation and conduction of nerve impulses in all types of neurons.

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63
Q

Q: What is the relationship between channel states and action potential propagation?

A

A: Channels open and close sequentially along the axon, allowing the action potential to move in one direction.

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64
Q

Q: How many Na+ ions typically flow into the cell when voltage-gated Na+ channels open?

A

A: Approximately 20,000 Na+ ions.

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65
Q

Q: What immediate effect does the influx of Na+ have on the membrane potential?

A

A: It significantly depolarizes the membrane, moving it toward a positive value.

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66
Q

Q: Why does the overall concentration of Na+ outside the cell remain nearly constant after the influx of Na+?

A

A: Because there are millions of Na+ ions present in the extracellular fluid.

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67
Q

Q: What role do sodium–potassium pumps play after Na+ enters the cell?

A

A: They quickly remove the 20,000 Na+ ions that entered, maintaining low Na+ concentration inside the cell.

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68
Q

Q: What is the significance of the rapid action of sodium–potassium pumps?

A

A: They help restore the resting membrane potential and ensure the cell is ready for the next action potential.

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69
Q

Q: What is action potential propagation?

A

A: The movement of the action potential along the axon, transmitting information down the neuron.

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70
Q

Q: What is the role of leaky K⁺ channels?

A

A: They allow potassium ions (K⁺) to move in and out of the axon, helping maintain the resting membrane potential by facilitating K⁺ exit.

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71
Q
A
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72
Q

Q: What happens when voltage-gated Na⁺ channels open?

A

A: Sodium ions (Na⁺) flow into the axon, contributing to depolarization.

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73
Q

Q: What marks the depolarization phase during an action potential?

A

A: The membrane potential reaches around +30 mV due to the influx of Na⁺ ions.

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74
Q

Q: How does the action potential lead to muscle contraction?

A

A: The action potential transmits signals to the muscle fibers at the neuromuscular junction, triggering contractions.

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75
Q

Q: What occurs during the propagation of an action potential?

A

A: More Na⁺ channels open sequentially, depolarizing each section of the membrane as the signal travels along the axon.

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76
Q

Q: What follows the depolarization phase in an action potential?

A
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77
Q

Q: How do ionic movements contribute to the generation of an action potential?

A

A: Na⁺ influx leads to depolarization, while K⁺ efflux helps to reset the membrane potential after the action potential.

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78
Q

Q: What happens at +30 mV during depolarization?

A

A: The inside of the axon becomes positive due to Na⁺ ion influx, driving the action potential down the axon.

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79
Q

Q: What triggers Ca2+ channels to open in synaptic end bulbs?

A

A: The arrival of a depolarizing nerve impulse.

80
Q

Q: What are synaptic vesicles?

A

A: Small sacs within neurons that store neurotransmitters, located in the presynaptic terminal.

81
Q

Q: How many neurotransmitter molecules can one vesicle hold?

A

A: Thousands of neurotransmitter molecules.

82
Q

Q: What is the sequence of events in neurotransmitter release?

A

A: 1. Ca2+ levels rise
2. Vesicles merge with membrane
3. Neurotransmitters release into synaptic cleft
4. Neurotransmitters bind to receptors

83
Q

Q: What happens when neurotransmitters bind to ligand-gated channels?

A

A: Channels open, allowing specific ions to flow, leading to either depolarization (Na+) or hyperpolarization (Cl- or K+).

84
Q

Q: What determines if a nerve impulse will be triggered in the postsynaptic neuron?

A

A: If depolarization reaches the threshold level.

85
Q

Q: What drives Ca2+ into the synaptic end bulb?

A

A: The concentration gradient (higher Ca2+ concentration in extracellular fluid).

86
Q

Q: What is the role of calcium in synaptic transmission?

A

A: It triggers synaptic vesicles to release neurotransmitters into the synaptic cleft.

87
Q

Q: What is the sequence of ACh release through exocytosis?

A

A: 1. Action potential arrives 2. Calcium channels open 3. Calcium enters neuron 4. Vesicles fuse with membrane 5. ACh releases into synaptic cleft

88
Q

Q: What are the two possible effects of ACh on postsynaptic neurons?

A

A:
1. Excitatory (EPSP) - depolarization
2. Inhibitory (IPSP) - hyperpolarization

89
Q

Q: How does ACh affect muscle cells?

A

A: It binds to receptors, opens ion channels, allows Na+ influx, triggers muscle contraction.

90
Q

Q: What is the role of acetylcholinesterase (AChE)?

A

A: It breaks down ACh into acetate and choline, stopping the signal and allowing reset.

91
Q

Q: What triggers calcium influx in the axon terminal?

A

A: The arrival of an action potential opening voltage-gated calcium channels.

92
Q

Q: What happens when ACh reaches the target cell?

A

A: 1. Diffuses across synaptic cleft 2. Binds to receptors 3. Opens ion channels 4. Triggers cellular response

93
Q

Q: What is an EPSP?

A

A: Excitatory postsynaptic potential - makes neuron more likely to reach action potential threshold.

94
Q

Q: What is an IPSP?

A

A: Inhibitory postsynaptic potential - makes it harder for neuron to reach threshold.

95
Q

Q: What happens when membrane reaches peak depolarization (+30mV)?

A

A: Voltage-gated Na+ channels automatically close (inactivate), preventing continuous action potentials.

96
Q

Q: What are the key steps in repolarization?

A

A: 1. Voltage-gated K+ channels open 2. Na+ channels close 3. K+ flows out of cell 4. Inside becomes more negative 5. Returns to resting potential (-70mV)

97
Q

Q: What is the after-hyperpolarizing phase?

A

A: Period when membrane potential becomes extra negative (around -90 mV) due to continued K+ outflow.

98
Q

Q: What are the two types of K+ channels involved in hyperpolarization?

A

A: 1. Voltage-gated K+ channels (respond to potential changes) 2. Leaky K+ channels (always slightly open)

99
Q

Q: What drives K+ outflow during hyperpolarization?

A

A: 1. Concentration gradient (more K+ inside)
2. Electrical gradient (negative inside)

100
Q

Q: What is the absolute refractory period?

A

A: Time when no stimulus can trigger another impulse, coinciding with Na+ channel inactivation.

101
Q

Q: How do Na+ and K+ channels differ in their inactivation?

A

A: Na+ channels have an inactivated state, while K+ channels simply open or close.

102
Q

Q: What is the typical voltage reached during hyperpolarization?

A

A: Around -90 mV (more negative than resting potential of -70 mV).

103
Q

Q: What are the three main mechanisms that reset a neuron after an action potential?

A

A: 1. Inactivation of Na⁺ channels 2. Opening of K⁺ channels 3. Action of Na⁺/K⁺ pump

104
Q

Q: How does the Na⁺/K⁺ pump reset ion concentrations?

A

A:
Pumps 3 Na⁺ ions out of cell
Pumps 2 K⁺ ions into cell
Uses active transport (ATP)

105
Q

Q: What is the role of voltage-gated Na⁺ channel inactivation?

A

A: Prevents further Na⁺ from entering the cell after depolarization.

106
Q

Q: How do K⁺ channels contribute to resetting?

A

A: They open during repolarization, allowing K⁺ to flow out, restoring negative membrane potential.

107
Q

Q: What is the end result of the reset process?

A

A: Return to resting membrane potential (-70 mV), preparing neuron for next action potential.

108
Q

Q: Why is the Na⁺/K⁺ pump considered an active transport mechanism?

A

A: It requires energy (ATP) to move ions against their concentration gradients.

109
Q

Q: What ion gradients are restored during reset?

A

A:
High Na⁺ outside, low inside
High K⁺ inside, low outside

110
Q

Q: What triggers the release of acetylcholine (ACh) at the neuromuscular junction?

A

A: The arrival of a nerve impulse, which opens voltage-gated calcium channels and allows calcium ions to enter the neuron.

111
Q

Q: What happens to ACh after it is released into the synaptic cleft?

A

A: ACh diffuses across the cleft and binds to receptors on the muscle cell’s membrane (sarcolemma).

112
Q

Q: What effect does ACh binding to muscle receptors have?

A

A: It opens ion channels, allowing sodium ions (Na⁺) to flow into the muscle cell, leading to depolarization.

113
Q

Q: What occurs if depolarization reaches the threshold in the muscle cell?

A

A: An action potential is generated, which travels along the muscle fiber’s membrane.

114
Q

Q: What is the role of calcium release from the sarcoplasmic reticulum?

A

A: It triggers muscle contraction in response to the action potential.

115
Q

Q: How is ACh’s action terminated in the synaptic cleft?

A

A: The enzyme acetylcholinesterase breaks down ACh, preventing continuous muscle stimulation.

116
Q

Q: Why is the breakdown of ACh important for muscle function?

A

A: It ensures that muscle contraction occurs in a regulated manner and prevents prolonged stimulation, allowing muscles to reset and be ready for the next signal.

117
Q

Q: What initiates the release of neurotransmitters at the synaptic end bulb?

A

A: The arrival of a nerve impulse that opens voltage-gated Ca²⁺ channels.

118
Q

Q: Why do calcium ions (Ca²⁺) flow into the presynaptic neuron?

A

A: Because they are more concentrated in the extracellular fluid compared to the inside of the neuron.

119
Q

Q: What does the increase in intracellular Ca²⁺ concentration trigger?

A

A: It triggers exocytosis of synaptic vesicles containing neurotransmitter molecules.

120
Q

Q: How do neurotransmitters reach the postsynaptic neuron?

A

A: They diffuse across the synaptic cleft after being released from synaptic vesicles.

121
Q

Q: What happens when neurotransmitters bind to receptors on ligand-gated channels?

A

A: The channels open, allowing specific ions to flow across the postsynaptic membrane.

122
Q

Q: What causes a postsynaptic potential to become depolarized?

A

A: The opening of Na⁺ channels, allowing Na⁺ to flow into the cell.

123
Q

Q: What can happen if Cl⁻ or K⁺ channels open in the postsynaptic membrane?

A

A: Opening Cl⁻ channels allows Cl⁻ to enter, causing hyperpolarization, while opening K⁺ channels allows K⁺ to exit, also leading to hyperpolarization.

124
Q

Q: What is the consequence of a depolarizing postsynaptic potential reaching threshold?

A

A: It triggers a nerve impulse in the axon of the postsynaptic neuron.

125
Q

Q: What is a postsynaptic potential?

A

A: The change in membrane voltage across the postsynaptic neuron in response to neurotransmitter binding.

126
Q

Q: What happens when acetylcholine (ACh) binds to receptors on muscle fibers?

A

A: Sodium (Na⁺) channels open, allowing Na⁺ ions to enter the muscle fiber.

127
Q

Q: What is the effect of sodium influx on the muscle fiber?

A

A: It causes depolarization of the muscle fiber membrane, leading to the generation of an action potential in the muscle cell.

128
Q

Q: What occurs when an action potential travels down the axon of a motor neuron?

A

A: It reaches the neuron’s terminal and triggers the opening of voltage-gated calcium (Ca²⁺) channels.

129
Q

Q: What role does calcium play in the neuromuscular junction?

A

A: The influx of calcium ions causes synaptic vesicles to release acetylcholine (ACh) into the synaptic cleft.

130
Q

Q: What happens after ACh is released into the synaptic cleft?

A

A: ACh binds to receptors on the muscle cell’s membrane (sarcolemma), leading to muscle contraction.

131
Q

Q: How does the action potential in the muscle cell lead to actual muscle contraction?

A

A: The depolarization initiated by sodium influx triggers a cascade of events that culminate in muscle contraction.

132
Q

Q: What is the primary function of axons in muscle control?

A

A: They transmit electrical signals from nerves to muscle fibers.

133
Q

Q: What is acetylcholine’s role in muscle function?

A

A: It acts as a chemical messenger between axons and muscle fibers.

134
Q

Q: What is a motor unit?

A

A: A motor neuron and all the muscle fibers that are connected to it.

135
Q

Q: What is the sarcolemma?

A

A: The cell membrane surrounding a muscle fiber that conducts electrical signals and allows ion exchange.

136
Q

Q: What are the primary ions exchanged across the sarcolemma during contraction?

A

A: Sodium and potassium ions.

137
Q

Q: What are the main functions of the sarcolemma?

A

A: 1. Conducts electrical signals 2. Allows ion exchange
3. Maintains muscle cell structure
4. Supports muscle cell function

138
Q

Q: What is the role of motor neurons?

A

A: They are nerve cells that connect to and control muscle fibers.

139
Q

Q: What happens when ACh binds to muscle fiber receptors?

A

A: It allows sodium ions (Na⁺) to enter the muscle cell, creating an action potential.

140
Q

Q: What are T-tubules?

A

A: Tube-like extensions of the muscle cell membrane that extend into the cell’s interior, carrying electrical signals deep into the muscle fiber.

141
Q

Q: What is the sarcoplasmic reticulum?

A

A: A specialized endoplasmic reticulum in muscle cells that stores and regulates calcium ions needed for muscle contraction.

142
Q

Q: What is the sequence of events in muscle activation?

A

A: 1. ACh release into synaptic cleft
2. ACh binding to receptors
3. Na⁺ influx
4. Action potential generation
5. Signal propagation through T-tubules
6. Calcium release from sarcoplasmic reticulum

143
Q

Q: What are the three main functions of the sarcoplasmic reticulum?

A

A: 1. Storage of calcium ions 2. Release of calcium for contraction 3. Reuptake of calcium for muscle relaxation

144
Q

Q: How do T-tubules contribute to muscle function?

A

A: They rapidly conduct action potentials from the surface to the interior of the muscle fiber.

145
Q

Q: What is the relationship between T-tubules and the sarcoplasmic reticulum?

A

A: T-tubules carry electrical signals that trigger the sarcoplasmic reticulum to release calcium for muscle contraction.

146
Q

Q: What happens after muscle contraction?

A

A: The sarcoplasmic reticulum pumps calcium back in, allowing the muscle to relax.

147
Q

Q: What are the four main stages of muscle activation?

A

A: 1. Initial Signal (ACh binding) 2. Signal Propagation (via T-tubules) 3. Calcium Release (from sarcoplasmic reticulum) 4. Muscle Response (contraction/relaxation)

148
Q

Q: What happens during the Initial Signal stage?

A

A:
- ACh binds to receptors

Sodium flows into muscle cell
Action potential generated

149
Q

Q: How is the signal propagated through the muscle fiber?

A

A: Action potential travels along membrane and through T-tubules, which carry it deep into the muscle fiber.

150
Q

Q: What triggers calcium release from the sarcoplasmic reticulum?

A

A: Voltage receptors in T-tubules detect the action potential and signal the sarcoplasmic reticulum to release calcium.

151
Q

Q: How is muscle stimulation terminated?

A

A: Acetylcholinesterase enzyme breaks down ACh, preventing continuous stimulation.

152
Q

Q: How does muscle relaxation occur?

A

A:
Calcium pumps activate

Use ATP energy

Actively transport Ca²⁺ back into sarcoplasmic reticulum

Muscle relaxes as calcium levels decrease

153
Q

Q: What role do calcium pumps play?

A

A: They use ATP to actively transport calcium ions from the muscle cell back into the sarcoplasmic reticulum for storage.

154
Q

Q: What is the importance of calcium storage in the sarcoplasmic reticulum?

A

A: Stored calcium can be quickly released for future muscle contractions when needed.

155
Q

Q: What triggers calcium release in muscle cells?

A

A: Action potentials activate voltage-sensitive receptors in T-tubules, causing the sarcoplasmic reticulum to release calcium ions.

156
Q

Q: What is sarcoplasm?

A

A: The fluid inside muscle cells, similar to cytoplasm, containing nutrients, organelles, and proteins needed for muscle contraction.

157
Q

Q: What is the sequence of events when calcium is released?

A

A:
1. Ca²⁺ binds to troponin
2. Troponin changes shape
3. Tropomyosin moves
4. Binding sites on actin exposed 5. Myosin can bind to actin

158
Q

Q: What is the role of troponin in muscle contraction?

A

A: It binds calcium ions and undergoes a structural change that moves tropomyosin away from actin binding sites.

159
Q

Q: What is tropomyosin’s function?

A

A: It normally covers binding sites on actin, preventing myosin binding until moved by calcium-activated troponin.

160
Q

Q: How do thin and thick filaments interact in muscle contraction?

A

A: When tropomyosin moves, myosin (thick filament) can bind to exposed sites on actin (thin filament).

161
Q

Q: What is the significance of exposing binding sites on actin?

A

A: It allows myosin heads to bind and initiate the cross-bridge cycle, leading to muscle contraction.

162
Q

Q: What components are involved in the first step of muscle contraction?

A

Calcium ions
Troponin
Tropomyosin
Actin (thin filaments)
Myosin (thick filaments)

163
Q

Q: What are the two main contractile proteins in muscles?

A

A: 1. Actin (thin filament) 2. Myosin (thick filament)

164
Q

Q: What is the role of actin in muscle contraction?

A

A:
Forms the backbone of contractile structure

Contains binding sites for myosin

Acts as a “track” for myosin movement

165
Q
A
166
Q

Q: What are the key features of myosin?

A

A:
Made of two parts wrapped together

  1. Has a “head” region that:
    - Binds to actin
    - Performs power stroke
  2. Composed of myosin heavy chains
167
Q

Q: What are the two main regulatory proteins?

A

A: 1. Troponin 2. Tropomyosin

168
Q

Q: What is the role of troponin?

A

A:
Binds to calcium ions

Changes shape when calcium binds

Controls tropomyosin’s position

169
Q

Q: What is the function of tropomyosin?

A

A:
Normally covers myosin binding sites on actin

Moves when troponin changes shape

Movement exposes binding sites for myosin

170
Q

Q: What is the sequence of the activation process?

A

A: 1. Calcium binds to troponin 2. Troponin changes shape 3. Tropomyosin shifts 4. Myosin binding sites exposed 5. Myosin heads bind to actin 6. Muscle contraction occurs

171
Q

Q: What is ATPase and its role?

A

A: An enzyme that breaks down ATP to provide energy for myosin movement along actin during contraction.

172
Q

Q: What is the primary function of actin in muscle contraction?

A

A: Acts as the backbone of the thin filament and contains binding sites for myosin.

173
Q

Q: Describe the structure of myosin.

A

A: Consists of two coiled heavy chains forming a tail with heads that bind to actin and perform power strokes.

174
Q

Q: What are the two main isoforms of myosin heavy chains, and what are their functions?

A

A: Type I: Found in slow-twitch fibers (endurance) Type II: Found in fast-twitch fibers (quick contraction)

175
Q

Q: How do troponin and tropomyosin regulate muscle contraction?

A

A: Troponin binds calcium, changes shape, and shifts tropomyosin to expose binding sites on actin.

176
Q

Q: What role do myosin heads play in muscle contraction?

A

A: They bind to actin and perform power strokes, essential for muscle contraction through ATP hydrolysis.

177
Q

Q: What triggers the movement of tropomyosin away from actin’s binding sites?

A

A: The binding of calcium to troponin causes this movement, enabling myosin binding.

178
Q

Q: Why is the regulation by troponin and tropomyosin essential?

A

A: They ensure that myosin binds to actin only when triggered by calcium, controlling muscle contraction.

179
Q

Contractile proteins

A

Proteins that generate force during muscle contractions.

180
Q

Regulatory proteins

A

Proteins that help switch muscle contraction process on and off.

181
Q

Q: What are the four stages of the cross-bridge cycle?

A

A: 1. Energizing Stage (ATP splitting) 2. Binding Stage (cross-bridge formation) 3. Power Stroke (force generation) 4. Reset Stage (return to start position)

182
Q

Q: Describe the sequence of events in muscle activation.

A

A: 1. Nerve action potential releases ACh 2. ACh binds to muscle receptors 3. Muscle action potential generated 4. Calcium released from SR 5. Calcium binds to troponin 6. Cross-bridge cycle begins

183
Q

Q: What happens during muscle relaxation?

A

A: 1. Calcium channels close 2. Ca²⁺-ATPase pumps calcium back into SR 3. Tropomyosin covers binding sites 4. Muscle returns to resting state

184
Q

Q: What occurs during the power stroke?

A

A:
Myosin head releases Pi
Head pivots from 90° to 45°
Pulls actin filament toward center
Generates force for contraction

185
Q

Q: How does the triad structure function?

A

A: Consists of one T-tubule and two SR ends, facilitating signal communication within muscle cells.

186
Q

Q: What role does ATP play in muscle function?

A

A: 1. Provides energy for myosin head movement 2. Enables release of myosin from actin 3. Powers calcium pumps during relaxation

187
Q

Q: How is continuous muscle contraction prevented?

A

A: Acetylcholinesterase breaks down ACh, stopping the signal unless more ACh is released.

188
Q

Q: What is the role of calcium in muscle regulation?

A

A:
Released from SR during stimulation
Binds to troponin
Enables myosin-actin binding
Removal causes relaxation

189
Q

Q: What are the two main mechanisms for ending muscle contraction?

A

A: 1. Calcium reuptake by Ca²⁺-ATPase pumps 2. Sodium-Potassium pump function

190
Q

Q: How does the Ca²⁺-ATPase pump work?

A

A:
Actively transports calcium back into sarcoplasmic reticulum
Uses ATP energy
Works against concentration gradient

191
Q

Q: What are the three main functions of calcium reuptake?

A

A: 1. Stops muscle contraction 2. Prepares muscle for next contraction 3. Maintains calcium storage in sarcoplasmic reticulum

192
Q

Q: How does the Sodium-Potassium pump restore balance?

A

Pumps 3 sodium ions out
Pumps 2 potassium ions in
Uses ATP for energy

193
Q

Q: What are the results of Sodium-Potassium pump action?

A

A: 1. Restores resting membrane potential 2. Creates conditions for next action potential 3. Maintains cell’s responsiveness

194
Q

Q: Why are both pump processes essential?

A

A: They enable:

Return to relaxed state
Preparation for next contraction
Maintenance of ion concentrations
Repeated muscle function

195
Q

Q: What triggers the need for calcium termination?

A

A: The need for muscle relaxation requires decrease of calcium levels in the sarcoplasm.

196
Q

Q: What energy source is required for both pumps?

A

A: ATP (adenosine triphosphate) powers both Ca²⁺-ATPase and Na⁺/K⁺ pumps.