Physio Ex Lab 3 Part 1 Key - PDF SGD2
Physio Ex Lab 3 Part 1 Key - PDF SGD2
Physio Ex Lab 3 Part 1 Key - PDF SGD2
Microelectrode position
Voltage (mV)
Control
Control
70
Control
Axon, extracellular
Control
Axon, intracellular
70
High K+
Axon, intracellular
40
High K+
Axon, extracellular
High K+
High K+
40
Low Na+
72
Low Na+
Low Na+
Axon, extracellular
Low Na+
Axon, intracellular
72
1. Explain why increasing extracellular K1 reduces the net diffusion of K1 out of the neuron through the K1
leak channels. Increasing the extracellular potassium reduces the steepness of the concentration gradient and
so less potassium diffuses out of the neuron.
2. Explain why increasing extracellular K1 causes the membrane potential to change to a less negative value.
How well did the results compare with your prediction? The membrane potential became less negative because
less potassium diffused out. If more potassium stays in, it is more positive or less negative.
3. Explain why a change in extracellular Na1 did not alter the membrane potential in the resting neuron. There
are less leakage sodium channels that leakage potassium channels, and more of the potassium channels are
open.
4. Discuss the relative permeability of the membrane to Na1 and K1 in a resting neuron. The resting neuron is
(45) times more permeable to potassium because of the increased number of leakage channels.
5. Discuss how a change in Na1 or K1 conductance would affect the resting membrane potential. A change in
the potassium conductance would have a greater effect on the resting membrane potential than a change in
sodium would.
Pacinian (lamellar)
corpuscle
Olfactory receptor
None
-70
-70
-70
Low
-60
-70
-70
Moderate
-45
-70
-70
High
-30
-70
-65
Low
-70
-64
-70
Moderate
-70
-58
-70
High
-70
-45
-70
Low
-70
-70
-60
Moderate
-70
-70
-40
High
-70
-70
-20
Low
-70
-70
-70
Moderate
-70
-70
-70
High
-70
-70
-70
Pressure
Chemical
Heat
Light
1. Sensory neurons have a resting potential based on the efflux of potassium ions (as demonstrated in Activity
1). What passive channels are likely found in the membrane of the olfactory receptor, in the membrane of the
Pacinian corpuscle, and in the membrane of the free nerve ending? The efflux of potassium ions is maintained
by passive potassium channels.
2. What is meant by the term graded potential? Graded potentials are brief, localized changes in the
membrane potential that can be either depolarizing or hyperpolarizing.
3. Identify which of the stimulus modalities induced the largest amplitude receptor potential in the Pacinian
corpuscle. How well did the results compare with your prediction? The moderate intensity pressure modality
induced a receptor potential of the largest amplitude in the Pacinian corpuscle.
4. Identify which of the stimulus modalities induced the largest-amplitude receptor potential in the olfactory
receptors. How well did the results compare with your prediction? The moderate intensity chemical modality
Peak value at R1
(V)
Action potential
10
No
20
100
100
Yes
30
100
100
Yes
40
100
100
Yes
50
100
100
Yes
1. Define the term threshold as it applies to an action potential. Threshold is the voltage that must be reached
in order to generate an action potential.
2. What change in membrane potential (depolarization or hyperpolarization) triggers an action potential? A
depolarization in the membrane potential results in an action potential. The membrane potential must become
less negative to generate an action potential.
3. How did the action potential at R1 (or R2) change as you increased the stimulus voltage above the threshold
voltage? How well did the results compare with your prediction? The action potential didnt change as the
stimulus voltage increased. This is because once threshold is met, the event is all or none, not graded.
4. An action potential is an all-or-nothing event. Explain what is meant by this phrase. This means that once
threshold is met an action potential occurs. If the stimulus is too small an action potential does not occur.
5. What part of a neuron was investigated in this activity? The trigger zone was investigated. This is where the
axon hillock and the initial segment come together.
Activity 4: The Action Potential: Importance of Voltage-Gated Na1 Channels (pp. 4244)
Peak value of response (V)
Condition
Stimulus
voltage (mV)
Electrode
s
2 sec
4 sec
6 sec
8 sec
10 sec
Control
30
R1
100
100
100
100
100
Control
30
R2
100
100
100
100
100
TTX
30
R1
100
100
100
100
100
TTX
30
R2
100
100
Lidocaine
30
R1
100
100
100
100
100
Lidocaine
30
R2
100
100
100
1. What does TTX do to voltage-gated Na1 channels? TTX blocks the diffusion of sodium through the voltagegated sodium channels.
2. What does lidocaine do to voltage-gated Na1 channels? How does the effect of lidocaine differ from the
effect of TTX? Lidocaine blocks the diffusion of sodium through the voltage-gated sodium channels.
3. A nerve is a bundle of axons, and some nerves are less sensitive to lidocaine. If a nerve, rather than an axon,
had been used in the lidocaine experiment, the responses recorded at R1 and R2 would be the sum of all the
action potentials (called a compound action potential). Would the response at R2 after lidocaine application
necessarily be zero? Why or why not? With a compound action potential, the results would not necessarily be
zero because some axons could remain unaffected.
4. Why are fewer action potentials recorded at R2 when TTX is applied between R1 and R2? How well did the
results compare with your prediction? TTX blocked the sodium channels, preventing the propagation of the
action potential from R1 to R2.
5. Why are fewer action potentials recorded at R2 when lidocaine is applied between R1 and R2? How well
did the results compare with your prediction? Lidocaine blocked the sodium channels, preventing the
propagation of the action potential from R1 to R2.
6. Pain-sensitive neurons (called nociceptors) conduct action potentials from the skin or teeth to sites in the
brain involved in pain perception. Where should a dentist inject the lidocaine to block pain perception?
Lidocaine should be applied to the receptors to prevent the generation of an action potential that would lead to
the perception of pain.