Download 13. What determines the magnitude of the graded potential? (p. 240)

ELECTRICAL SIGNALS
Electrical communication will be the topic of the next few sections as we cover the
Nervous System. The Nervous System is specialized for rapid communication of signals
throughout the body, and is composed of two primary cell types: neurons and glial cells.
Neurons are responsible for producing and transmitting electrical and chemical signals to
cells throughout the body, whereas glial cells are the support cells for the system. We
will focus our attention on neurons, which have three basic parts: the cell body, the axon,
and the dendrites.
As you have learned, electrical signaling along the neuron is due to ion movement across
its membrane. Different portions of the neuron conduct electrical signals differently.
The conduction of action potentials occurs only on the axon. The cell body and dendrites
lack the fast Na+ channels necessary for the initiation of an action potential, and instead
exhibit smaller electrical changes called graded potentials. Graded potentials are
summed, and if they surpass the threshold for the membrane, an action potential is
created. Action potentials cannot be summed, and are called “all or none” phenomena.
I assume you know basic neuronal anatomy!
ELECTRICAL SIGNALS IN NEURONS
1. Neurons and muscle cells are called excitable tissues because
they do what? (p. 236)
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2. What two factors influence membrane potential? (p. 236)
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3. _________ is the major ion contributing to the resting
membrane potential.
4. Which ion is more concentrated in the ECF: Na+ or K+ ?
Which is more concentrated in the ICF?
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5. If the cell membrane is made suddenly permeable to Na+, in
which direction will it move? What is causing this movement?
(p. 238)
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6. When the membrane potential moves from –70 mV to +10 mV,
what happens to the existing concentration differences across
the membrane? (p. 238)
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7.
If the cell membrane suddenly becomes more permeable to
K+, what happens to the state of the membrane? Why?
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8. How do cells alter their permeability to ions? (p. 238-39)
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9. How are ion channels classified? Describe each type briefly
(p. 239)
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10. What is a graded potential? (p. 240)
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11. How are action potentials different from graded potentials?
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12. Where on the neuron do graded potentials occur? Action
potentials? (p. 240-41)
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13. What determines the magnitude of the graded potential? (p. 240)
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14. Describe two ways in which ion movement can hyperpolarize a cell.
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15. Where is the trigger zone? (p. 241)
________________________________________
16. If a graded potential reaches threshold at the trigger zone, what
happens? (p. 241-42)
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________________________________________________________________
17. If several graded potentials reach the trigger zone at the same
time, what do you think will happen? Explain.
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18. Define an action potential. (p. 242)
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19. What does “all-or-none” mean when referring to action
potentials? (p. 242)
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20. Action potentials specifically involve the movements of what
two ions? In which direction are they moving? (p. 243)
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________________________________________________________________
21. For each phase of the action potential listed below, indicate
what is happening to ion permeability, which ions are moving,
and in what direction (in or out of cell).
Rising phase:
Peak:
Falling phase:
After-hyperpolarization:
22. Name the two gates of the voltage-gated Na+ channels. (p. 245)
______________________________________________________
23. In the resting neuron, which of these gates are closed and
which are open?
______________________________________________________
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24. Depolarization opens the _____________________________
gate.
25. When do inactivation gates close? Why do they close? (p. 245)
______________________________________________________
________________________________________________________________
26. What must happen to the gates before the next action potential
can take place?
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27. Define refractory period. (p. 245-46)
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28. How do the absolute & relative refractory periods differ?
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29. Why might the absolute refractory period be a “good thing”?
(p. 246)
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30. Describe the role of the Na+/K+ ATPase pump in the action
potential. (p. 246)
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31. What is meant by the conduction of action potentials? (p. 246)
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32. When Na+ channels in the middle of an axon open,
depolarizing current flow will spread in both directions along
the axon. Why then don’t action potentials ever reverse and
move back toward the cell body?
______________________________________________________
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______________________________________________________
33. List two factors that affect the speed of action potential
conduction. (p. 247-49)
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34. Explain saltatory conduction. (p. 249)
______________________________________________________
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35. What happens to conduction through axons that have lost their
myelin? (p. 249)
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THINGS TO TRY:
1. Lidocaine inactivates voltage-gated Na+ channels on the neuronal membrane. If
lidocaine is placed on the axon of a nerve that normally transmits signals from a
pain receptor to the brain (to be interpreted by the brain as “pain”), the pain is not
“felt” by the individual. Explain why.
2. Draw/label a neuron. Indicate on your picture exactly where graded
potentials would be generated and where action potentials would be generated
3. Drug Z prevents sodium inactivation (“h”) gates from moving from their resting
position (“resting” refers to their position when the membrane is at its RMP).
How would administration of Drug Z affect the function of a neuron?
SYNAPSES
READING: p. 253-
An action potential can travel down the length of the neuronal membrane and
communicate the electrical information to another cell. This transmission occurs via a
synapse. A synapse is a junction between a neuron and a target cell, which could be
another neuron, a muscle cell, or a gland. At a synapse, the axon of the presynaptic
neuron passes information to receptors on the dendrites or cell body of the postsynaptic
target cell(s). Most synapses are chemical junctions, and involve the release of
neurotransmitter from the presynaptic neuron onto the postsynaptic cell.
Neurotransmitters are manufactured in the cell bodies of neurons (where the organelles
are located) and travel down to the axon terminal where they are housed in vesicles until
signaled for release. When the appropriate signal (action potential) arrives,
neurotransmitter is released via exocytosis. The neurotransmitter then travels by
diffusion to the postsynaptic membrane where it opens ion channels, resulting in some
type of electrical potential change. Because this electrical change occurs on the dendrites
or cell body, it is a graded potential. The overall postsynaptic potential change will
determine whether or not an action potential will be fired.
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Synaptic transmissions that bring the postsynaptic membrane closer to threshold are
called excitatory postsynaptic potentials, or EPSPs. Inhibitory postsynaptic potentials, or
IPSPs, take the membrane further from threshold. As mentioned, it is the overall
postsynaptic potential that will determine if an action potential is fired on the
postsynaptic cell.
1.
Name the seven classes of neurotransmitters. (p. 254-57)
______________________________________________________
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*Note: we will spend a lot of time in class on specific NT’s, so
just read over the info on pg. 255 to get familiar with them.
2.
What are the possible places for neurotransmitter
synthesis? Where is it stored? (p. 257)
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3. At a chemical synapse, describe the sequence of events that
leads to neurotransmitter release, beginning with an action
potential traveling along the presynaptic membrane. (p. 258)
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4. What is the chemical trigger for neurotransmitter release?
______________________________________________________
5. How does the new “kiss and run” pathway compare to regular
exocytosis? (p. 258)
______________________________________________________
6. What happens to Ach after it is released into the synaptic cleft?
(Fig. 8-19, p. 259)
______________________________________________________
7. How, using the same neurotransmitter, might an olfactory
neuron alert you to a stronger smell? (p. 260)
______________________________________________________
8. Draw a picture of neurons converging and another of neurons
diverging. (p. 262)
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9. Name one advantage of convergence. (Fig. 8-22, p. 262)
______________________________________________________
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10. A slow synaptic potential would likely cause what type of
effect? (Fig 8-23, p. 263)
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11. What is spatial summation of graded potentials? (p. 264-65)
______________________________________________________
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12. Describe postsynaptic inhibition (p. 266)
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13. Describe temporal summation (Fig. 8-24, p. 264)
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14. Define long-term potentiation (p. 267)
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15. When might long-term potentiation be useful?
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16. List some pharmacological agents that can alter synaptic
transmission. (p. 268)
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17. Neuron A, Neuron B and Neuron C are all presynaptic to
Neuron F. If A and B fire, F fires. If A and C fire, nothing
happens. Draw this scenario below.
What can you conclude about the synapse between C and F?
Between A and F? What other information might you need?
______________________________________________________
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18. Neuron J, Neuron K, and Neuron L are all presynaptic to
Neuron T. J and K are both excitatory to T, whereas L is
inhibitory to T. Assume that T needs a net input of +2 (one
EPSP is +1; one IPSP is -1) to fire an action potential.
Describe how temporal summation could result in an action
potential on T. Describe how spatial summation could result in
an action potential on T.
______________________________________________________
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THINGS TO TRY:
1. Neuron A, Neuron B and Neuron C are presynaptic to Neuron D. When A fires an
action potential, D fires an action potential. When A and B fire simultaneously, D
does not fire. When A, B, and C fire simultaneously, D fires. This is an example
of...
A. inhibition by D and temporal summation by A and B.
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B. inhibition by B and temporal summation by A and C.
C. inhibition by B and spatial summation by A and C.
D. inhibition by B and spatial summation by A and D.
E. inhibition by A and spatial summation by B and C.
Defend your choice.
2. Black widow venom causes an explosive release in acetylcholine from the axon
terminals of neurons leading to skeletal muscle. Discuss why this might be
problematic to the victim.
3. Botulism toxin blocks the release of acetylcholine from these same neurons.
How would the effects of this toxin compare to black widow venom? Can you
explain why the victim would experience respiratory distress in both cases?
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