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.
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.
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.
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.
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.
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.
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.
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.
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.
10
Q
Q: How are ion concentrations distributed at rest?
A
A: K+ is more concentrated inside the neuron; Na+ is more concentrated outside.
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.
12
Q
Q: What happens during depolarization?
A
A: Voltage-gated Na+ channels open, allowing Na+ to rush in, making the inside more positive.
13
Q
Q: How does repolarization occur?
A
A: Voltage-gated K+ channels open, allowing K+ to flow out, restoring the negative membrane potential.
14
Q
Q: What triggers neurotransmitter release at the neuromuscular junction?
A
A: An action potential reaching the axon terminal.
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.
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
17
Q
Q: What neurotransmitter is released at the neuromuscular junction?
A
Acetylcholine
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.
19
Q
Q: What ions are primarily found in extracellular fluid?
A
A: High concentrations of sodium (Na+) and chloride (Cl−).
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).
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.
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.
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.
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.
25
Q: What effect does the Na+/K+ pump have on the neuron’s negativity?
A: Its activity contributes about -3 mV of the total resting potential of -70 mV.
26
Q: What happens during depolarization when a neuron is stimulated?
A: Sodium channels open, allowing Na+ to enter the neuron, moving the charge closer to the action potential threshold.
27
Q: What is the importance of the Na+/K+ pump after an action potential?
A: It restores the resting potential by removing excess Na+ and bringing K+ back into the neuron.
28
Q: What are the four types of ion channels?
A:
1. Leak channels
2. Ligand-gated channels
3. Mechanically gated channels 4. Voltage-gated channels
29
Q: What are the characteristics of leak channels?
A:
- Open and close randomly
- More K+ channels than Na+ channels
- Found in all cells
30
Q: What triggers ligand-gated channels?
A: Chemical signals like neurotransmitters or hormones.
31
Q: What activates mechanically gated channels?
A: Physical forces like touch, pressure, or stretching.
32
Q: What is the critical threshold for an action potential?
A: -55 millivolts.
33
Q: How does the Na+/K+ pump maintain ion gradients?
A: It moves 3 Na+ out for every 2 K+ in, using ATP for energy.
34
Q: Describe the charge distribution across the membrane:
A: Outside: More positive, high Na+, lower K+ Inside: More negative, high K+, lower Na+, negative proteins
35
Q: What drives sodium rush during an action potential?
A: The electrochemical gradient (concentration difference and electrical attraction).
36
Q: How do leaky K+ channels affect membrane potential?
A: They allow continuous K+ outflow, creating a negative interior (-70mV).
37
Q: What is the purpose of this ion channel system?
A: To ensure:
Stable resting potential
Ready for action potentials
Consistent cellular function
Proper neural signaling
38
Q: What creates an electrochemical gradient?
A: The combination of:
Concentration gradient (ion concentration differences)
Electrical gradient (charge differences across membrane)
39
Q: What is the resting membrane potential?
A: The electrical charge difference (-70 mV) across a neuron's membrane when not sending signals.
40
Q: What are the main phases of an action potential?
A: 1. Depolarizing phase 2. Repolarizing phase 3. After-hyperpolarizing phase
41
Q: How do Na+ ions behave in neurons?
A: - Higher concentration outside cell
Flow inward when channels open
Attracted by negative internal charge
42
Q: How do K+ ions behave in neurons?
A: - Higher concentration inside cell
Tend to move outward
Movement limited by internal negative proteins
43
Q: What is the threshold for an action potential?
A: -55 mV; depolarization must reach this level to trigger an action potential.
44
Q: What is the "all-or-none" principle?
A: Action potentials occur at full strength or not at all, regardless of stimulus strength.
45
Q: How do stronger stimuli affect nerve impulses?
A: They increase frequency of action potentials, not their intensity.
46
Q: What happens during depolarization?
A: Membrane potential becomes less negative, reaches zero, then becomes positive due to Na+ influx.
47
Q: What happens during repolarization?
A: Membrane potential returns to -70 mV as K+ channels open and K+ flows out.
48
Q: What membrane potential triggers an action potential?
A: -55 mV (threshold potential)
49
Q: What is the sequence of events after reaching threshold?
A: 1. Voltage-gated Na+ channels open 2. Rapid Na+ influx 3. Depolarization begins 4. Positive feedback loop 5. Action potential generation
50
Q: What is the peak voltage typically reached during an action potential?
A: Around +30 mV
51
Q: What is the positive feedback loop in action potential generation?
A: Na+ influx causes more voltage-gated Na+ channels to open, leading to further depolarization.
52
Q: How does repolarization begin?
A: Na+ channels close and voltage-gated K+ channels open.
53
Q: What is the purpose of depolarization?
A: To generate an action potential that can propagate along the axon.
54
Q: What drives the rapid change in membrane potential?
A: The sudden influx of Na+ ions through voltage-gated channels.
55
Q: What happens to the membrane potential during depolarization?
A: It becomes less negative and moves toward positive values.
56
Q: How does an action potential propagate along an axon?
A: It moves as a wave of depolarization, with voltage-gated Na⁺ channels opening sequentially to allow Na⁺ influx.
57
Q: What is the role of leaky K⁺ channels?
A: They allow K⁺ to continuously leak out of the axon, helping maintain the resting membrane potential.
58
Q: What triggers voltage-gated channels to open?
A: Changes in membrane potential (voltage).
59
Q: How many gates does each voltage-gated Na+ channel have?
A: Two gates: an activation gate and an inactivation gate.
60
Q: What is the state of Na+ channel gates at rest?
A: Inactivation gate is open, activation gate is closed, preventing Na+ entry.
61
Q: What happens to Na+ channel gates at threshold?
A: Both activation and inactivation gates open, allowing Na+ inflow.
62
Q: Why are voltage-gated channels important?
A: They participate in the generation and conduction of nerve impulses in all types of neurons.
63
Q: What is the relationship between channel states and action potential propagation?
A: Channels open and close sequentially along the axon, allowing the action potential to move in one direction.
64
Q: How many Na+ ions typically flow into the cell when voltage-gated Na+ channels open?
A: Approximately 20,000 Na+ ions.
65
Q: What immediate effect does the influx of Na+ have on the membrane potential?
A: It significantly depolarizes the membrane, moving it toward a positive value.
66
Q: Why does the overall concentration of Na+ outside the cell remain nearly constant after the influx of Na+?
A: Because there are millions of Na+ ions present in the extracellular fluid.
67
Q: What role do sodium–potassium pumps play after Na+ enters the cell?
A: They quickly remove the 20,000 Na+ ions that entered, maintaining low Na+ concentration inside the cell.
68
Q: What is the significance of the rapid action of sodium–potassium pumps?
A: They help restore the resting membrane potential and ensure the cell is ready for the next action potential.
69
Q: What is action potential propagation?
A: The movement of the action potential along the axon, transmitting information down the neuron.
70
Q: What is the role of leaky K⁺ channels?
A: They allow potassium ions (K⁺) to move in and out of the axon, helping maintain the resting membrane potential by facilitating K⁺ exit.
71
72
Q: What happens when voltage-gated Na⁺ channels open?
A: Sodium ions (Na⁺) flow into the axon, contributing to depolarization.
73
Q: What marks the depolarization phase during an action potential?
A: The membrane potential reaches around +30 mV due to the influx of Na⁺ ions.
74
Q: How does the action potential lead to muscle contraction?
A: The action potential transmits signals to the muscle fibers at the neuromuscular junction, triggering contractions.
75
Q: What occurs during the propagation of an action potential?
A: More Na⁺ channels open sequentially, depolarizing each section of the membrane as the signal travels along the axon.
76
Q: What follows the depolarization phase in an action potential?
77
Q: How do ionic movements contribute to the generation of an action potential?
A: Na⁺ influx leads to depolarization, while K⁺ efflux helps to reset the membrane potential after the action potential.
78
Q: What happens at +30 mV during depolarization?
A: The inside of the axon becomes positive due to Na⁺ ion influx, driving the action potential down the axon.
79
Q: What triggers Ca2+ channels to open in synaptic end bulbs?
A: The arrival of a depolarizing nerve impulse.
80
Q: What are synaptic vesicles?
A: Small sacs within neurons that store neurotransmitters, located in the presynaptic terminal.
81
Q: How many neurotransmitter molecules can one vesicle hold?
A: Thousands of neurotransmitter molecules.
82
Q: What is the sequence of events in neurotransmitter release?
A: 1. Ca2+ levels rise
2. Vesicles merge with membrane
3. Neurotransmitters release into synaptic cleft
4. Neurotransmitters bind to receptors
83
Q: What happens when neurotransmitters bind to ligand-gated channels?
A: Channels open, allowing specific ions to flow, leading to either depolarization (Na+) or hyperpolarization (Cl- or K+).
84
Q: What determines if a nerve impulse will be triggered in the postsynaptic neuron?
A: If depolarization reaches the threshold level.
85
Q: What drives Ca2+ into the synaptic end bulb?
A: The concentration gradient (higher Ca2+ concentration in extracellular fluid).
86
Q: What is the role of calcium in synaptic transmission?
A: It triggers synaptic vesicles to release neurotransmitters into the synaptic cleft.
87
Q: What is the sequence of ACh release through exocytosis?
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: What are the two possible effects of ACh on postsynaptic neurons?
A:
1. Excitatory (EPSP) - depolarization
2. Inhibitory (IPSP) - hyperpolarization
89
Q: How does ACh affect muscle cells?
A: It binds to receptors, opens ion channels, allows Na+ influx, triggers muscle contraction.
90
Q: What is the role of acetylcholinesterase (AChE)?
A: It breaks down ACh into acetate and choline, stopping the signal and allowing reset.
91
Q: What triggers calcium influx in the axon terminal?
A: The arrival of an action potential opening voltage-gated calcium channels.
92
Q: What happens when ACh reaches the target cell?
A: 1. Diffuses across synaptic cleft 2. Binds to receptors 3. Opens ion channels 4. Triggers cellular response
93
Q: What is an EPSP?
A: Excitatory postsynaptic potential - makes neuron more likely to reach action potential threshold.
94
Q: What is an IPSP?
A: Inhibitory postsynaptic potential - makes it harder for neuron to reach threshold.
95
Q: What happens when membrane reaches peak depolarization (+30mV)?
A: Voltage-gated Na+ channels automatically close (inactivate), preventing continuous action potentials.
96
Q: What are the key steps in repolarization?
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: What is the after-hyperpolarizing phase?
A: Period when membrane potential becomes extra negative (around -90 mV) due to continued K+ outflow.
98
Q: What are the two types of K+ channels involved in hyperpolarization?
A: 1. Voltage-gated K+ channels (respond to potential changes) 2. Leaky K+ channels (always slightly open)
99
Q: What drives K+ outflow during hyperpolarization?
A: 1. Concentration gradient (more K+ inside)
2. Electrical gradient (negative inside)
100
Q: What is the absolute refractory period?
A: Time when no stimulus can trigger another impulse, coinciding with Na+ channel inactivation.
101
Q: How do Na+ and K+ channels differ in their inactivation?
A: Na+ channels have an inactivated state, while K+ channels simply open or close.
102
Q: What is the typical voltage reached during hyperpolarization?
A: Around -90 mV (more negative than resting potential of -70 mV).
103
Q: What are the three main mechanisms that reset a neuron after an action potential?
A: 1. Inactivation of Na⁺ channels 2. Opening of K⁺ channels 3. Action of Na⁺/K⁺ pump
104
Q: How does the Na⁺/K⁺ pump reset ion concentrations?
A:
Pumps 3 Na⁺ ions out of cell
Pumps 2 K⁺ ions into cell
Uses active transport (ATP)
105
Q: What is the role of voltage-gated Na⁺ channel inactivation?
A: Prevents further Na⁺ from entering the cell after depolarization.
106
Q: How do K⁺ channels contribute to resetting?
A: They open during repolarization, allowing K⁺ to flow out, restoring negative membrane potential.
107
Q: What is the end result of the reset process?
A: Return to resting membrane potential (-70 mV), preparing neuron for next action potential.
108
Q: Why is the Na⁺/K⁺ pump considered an active transport mechanism?
A: It requires energy (ATP) to move ions against their concentration gradients.
109
Q: What ion gradients are restored during reset?
A:
High Na⁺ outside, low inside
High K⁺ inside, low outside
110
Q: What triggers the release of acetylcholine (ACh) at the neuromuscular junction?
A: The arrival of a nerve impulse, which opens voltage-gated calcium channels and allows calcium ions to enter the neuron.
111
Q: What happens to ACh after it is released into the synaptic cleft?
A: ACh diffuses across the cleft and binds to receptors on the muscle cell’s membrane (sarcolemma).
112
Q: What effect does ACh binding to muscle receptors have?
A: It opens ion channels, allowing sodium ions (Na⁺) to flow into the muscle cell, leading to depolarization.
113
Q: What occurs if depolarization reaches the threshold in the muscle cell?
A: An action potential is generated, which travels along the muscle fiber's membrane.
114
Q: What is the role of calcium release from the sarcoplasmic reticulum?
A: It triggers muscle contraction in response to the action potential.
115
Q: How is ACh's action terminated in the synaptic cleft?
A: The enzyme acetylcholinesterase breaks down ACh, preventing continuous muscle stimulation.
116
Q: Why is the breakdown of ACh important for muscle function?
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: What initiates the release of neurotransmitters at the synaptic end bulb?
A: The arrival of a nerve impulse that opens voltage-gated Ca²⁺ channels.
118
Q: Why do calcium ions (Ca²⁺) flow into the presynaptic neuron?
A: Because they are more concentrated in the extracellular fluid compared to the inside of the neuron.
119
Q: What does the increase in intracellular Ca²⁺ concentration trigger?
A: It triggers exocytosis of synaptic vesicles containing neurotransmitter molecules.
120
Q: How do neurotransmitters reach the postsynaptic neuron?
A: They diffuse across the synaptic cleft after being released from synaptic vesicles.
121
Q: What happens when neurotransmitters bind to receptors on ligand-gated channels?
A: The channels open, allowing specific ions to flow across the postsynaptic membrane.
122
Q: What causes a postsynaptic potential to become depolarized?
A: The opening of Na⁺ channels, allowing Na⁺ to flow into the cell.
123
Q: What can happen if Cl⁻ or K⁺ channels open in the postsynaptic membrane?
A: Opening Cl⁻ channels allows Cl⁻ to enter, causing hyperpolarization, while opening K⁺ channels allows K⁺ to exit, also leading to hyperpolarization.
124
Q: What is the consequence of a depolarizing postsynaptic potential reaching threshold?
A: It triggers a nerve impulse in the axon of the postsynaptic neuron.
125
Q: What is a postsynaptic potential?
A: The change in membrane voltage across the postsynaptic neuron in response to neurotransmitter binding.
126
Q: What happens when acetylcholine (ACh) binds to receptors on muscle fibers?
A: Sodium (Na⁺) channels open, allowing Na⁺ ions to enter the muscle fiber.
127
Q: What is the effect of sodium influx on the muscle fiber?
A: It causes depolarization of the muscle fiber membrane, leading to the generation of an action potential in the muscle cell.
128
Q: What occurs when an action potential travels down the axon of a motor neuron?
A: It reaches the neuron's terminal and triggers the opening of voltage-gated calcium (Ca²⁺) channels.
129
Q: What role does calcium play in the neuromuscular junction?
A: The influx of calcium ions causes synaptic vesicles to release acetylcholine (ACh) into the synaptic cleft.
130
Q: What happens after ACh is released into the synaptic cleft?
A: ACh binds to receptors on the muscle cell's membrane (sarcolemma), leading to muscle contraction.
131
Q: How does the action potential in the muscle cell lead to actual muscle contraction?
A: The depolarization initiated by sodium influx triggers a cascade of events that culminate in muscle contraction.
132
Q: What is the primary function of axons in muscle control?
A: They transmit electrical signals from nerves to muscle fibers.
133
Q: What is acetylcholine's role in muscle function?
A: It acts as a chemical messenger between axons and muscle fibers.
134
Q: What is a motor unit?
A: A motor neuron and all the muscle fibers that are connected to it.
135
Q: What is the sarcolemma?
A: The cell membrane surrounding a muscle fiber that conducts electrical signals and allows ion exchange.
136
Q: What are the primary ions exchanged across the sarcolemma during contraction?
A: Sodium and potassium ions.
137
Q: What are the main functions of the sarcolemma?
A: 1. Conducts electrical signals 2. Allows ion exchange
3. Maintains muscle cell structure
4. Supports muscle cell function
138
Q: What is the role of motor neurons?
A: They are nerve cells that connect to and control muscle fibers.
139
Q: What happens when ACh binds to muscle fiber receptors?
A: It allows sodium ions (Na⁺) to enter the muscle cell, creating an action potential.
140
Q: What are T-tubules?
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: What is the sarcoplasmic reticulum?
A: A specialized endoplasmic reticulum in muscle cells that stores and regulates calcium ions needed for muscle contraction.
142
Q: What is the sequence of events in muscle activation?
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: What are the three main functions of the sarcoplasmic reticulum?
A: 1. Storage of calcium ions 2. Release of calcium for contraction 3. Reuptake of calcium for muscle relaxation
144
Q: How do T-tubules contribute to muscle function?
A: They rapidly conduct action potentials from the surface to the interior of the muscle fiber.
145
Q: What is the relationship between T-tubules and the sarcoplasmic reticulum?
A: T-tubules carry electrical signals that trigger the sarcoplasmic reticulum to release calcium for muscle contraction.
146
Q: What happens after muscle contraction?
A: The sarcoplasmic reticulum pumps calcium back in, allowing the muscle to relax.
147
Q: What are the four main stages of muscle activation?
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: What happens during the Initial Signal stage?
A:
- ACh binds to receptors
Sodium flows into muscle cell
Action potential generated
149
Q: How is the signal propagated through the muscle fiber?
A: Action potential travels along membrane and through T-tubules, which carry it deep into the muscle fiber.
150
Q: What triggers calcium release from the sarcoplasmic reticulum?
A: Voltage receptors in T-tubules detect the action potential and signal the sarcoplasmic reticulum to release calcium.
151
Q: How is muscle stimulation terminated?
A: Acetylcholinesterase enzyme breaks down ACh, preventing continuous stimulation.
152
Q: How does muscle relaxation occur?
A:
Calcium pumps activate
Use ATP energy
Actively transport Ca²⁺ back into sarcoplasmic reticulum
Muscle relaxes as calcium levels decrease
153
Q: What role do calcium pumps play?
A: They use ATP to actively transport calcium ions from the muscle cell back into the sarcoplasmic reticulum for storage.
154
Q: What is the importance of calcium storage in the sarcoplasmic reticulum?
A: Stored calcium can be quickly released for future muscle contractions when needed.
155
Q: What triggers calcium release in muscle cells?
A: Action potentials activate voltage-sensitive receptors in T-tubules, causing the sarcoplasmic reticulum to release calcium ions.
156
Q: What is sarcoplasm?
A: The fluid inside muscle cells, similar to cytoplasm, containing nutrients, organelles, and proteins needed for muscle contraction.
157
Q: What is the sequence of events when calcium is released?
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: What is the role of troponin in muscle contraction?
A: It binds calcium ions and undergoes a structural change that moves tropomyosin away from actin binding sites.
159
Q: What is tropomyosin's function?
A: It normally covers binding sites on actin, preventing myosin binding until moved by calcium-activated troponin.
160
Q: How do thin and thick filaments interact in muscle contraction?
A: When tropomyosin moves, myosin (thick filament) can bind to exposed sites on actin (thin filament).
161
Q: What is the significance of exposing binding sites on actin?
A: It allows myosin heads to bind and initiate the cross-bridge cycle, leading to muscle contraction.
162
Q: What components are involved in the first step of muscle contraction?
Calcium ions
Troponin
Tropomyosin
Actin (thin filaments)
Myosin (thick filaments)
163
Q: What are the two main contractile proteins in muscles?
A: 1. Actin (thin filament) 2. Myosin (thick filament)
164
Q: What is the role of actin in muscle contraction?
A:
Forms the backbone of contractile structure
Contains binding sites for myosin
Acts as a "track" for myosin movement
165
166
Q: What are the key features of myosin?
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: What are the two main regulatory proteins?
A: 1. Troponin 2. Tropomyosin
168
Q: What is the role of troponin?
A:
Binds to calcium ions
Changes shape when calcium binds
Controls tropomyosin's position
169
Q: What is the function of tropomyosin?
A:
Normally covers myosin binding sites on actin
Moves when troponin changes shape
Movement exposes binding sites for myosin
170
Q: What is the sequence of the activation process?
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: What is ATPase and its role?
A: An enzyme that breaks down ATP to provide energy for myosin movement along actin during contraction.
172
Q: What is the primary function of actin in muscle contraction?
A: Acts as the backbone of the thin filament and contains binding sites for myosin.
173
Q: Describe the structure of myosin.
A: Consists of two coiled heavy chains forming a tail with heads that bind to actin and perform power strokes.
174
Q: What are the two main isoforms of myosin heavy chains, and what are their functions?
A: Type I: Found in slow-twitch fibers (endurance) Type II: Found in fast-twitch fibers (quick contraction)
175
Q: How do troponin and tropomyosin regulate muscle contraction?
A: Troponin binds calcium, changes shape, and shifts tropomyosin to expose binding sites on actin.
176
Q: What role do myosin heads play in muscle contraction?
A: They bind to actin and perform power strokes, essential for muscle contraction through ATP hydrolysis.
177
Q: What triggers the movement of tropomyosin away from actin's binding sites?
A: The binding of calcium to troponin causes this movement, enabling myosin binding.
178
Q: Why is the regulation by troponin and tropomyosin essential?
A: They ensure that myosin binds to actin only when triggered by calcium, controlling muscle contraction.
179
Contractile proteins
Proteins that generate force during muscle contractions.
180
Regulatory proteins
Proteins that help switch muscle contraction process on and off.
181
Q: What are the four stages of the cross-bridge cycle?
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: Describe the sequence of events in muscle activation.
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: What happens during muscle relaxation?
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: What occurs during the power stroke?
A:
Myosin head releases Pi
Head pivots from 90° to 45°
Pulls actin filament toward center
Generates force for contraction
185
Q: How does the triad structure function?
A: Consists of one T-tubule and two SR ends, facilitating signal communication within muscle cells.
186
Q: What role does ATP play in muscle function?
A: 1. Provides energy for myosin head movement 2. Enables release of myosin from actin 3. Powers calcium pumps during relaxation
187
Q: How is continuous muscle contraction prevented?
A: Acetylcholinesterase breaks down ACh, stopping the signal unless more ACh is released.
188
Q: What is the role of calcium in muscle regulation?
A:
Released from SR during stimulation
Binds to troponin
Enables myosin-actin binding
Removal causes relaxation
189
Q: What are the two main mechanisms for ending muscle contraction?
A: 1. Calcium reuptake by Ca²⁺-ATPase pumps 2. Sodium-Potassium pump function
190
Q: How does the Ca²⁺-ATPase pump work?
A:
Actively transports calcium back into sarcoplasmic reticulum
Uses ATP energy
Works against concentration gradient
191
Q: What are the three main functions of calcium reuptake?
A: 1. Stops muscle contraction 2. Prepares muscle for next contraction 3. Maintains calcium storage in sarcoplasmic reticulum
192
Q: How does the Sodium-Potassium pump restore balance?
Pumps 3 sodium ions out
Pumps 2 potassium ions in
Uses ATP for energy
193
Q: What are the results of Sodium-Potassium pump action?
A: 1. Restores resting membrane potential 2. Creates conditions for next action potential 3. Maintains cell's responsiveness
194
Q: Why are both pump processes essential?
A: They enable:
Return to relaxed state
Preparation for next contraction
Maintenance of ion concentrations
Repeated muscle function
195
Q: What triggers the need for calcium termination?
A: The need for muscle relaxation requires decrease of calcium levels in the sarcoplasm.
196
Q: What energy source is required for both pumps?
A: ATP (adenosine triphosphate) powers both Ca²⁺-ATPase and Na⁺/K⁺ pumps.
