190
Chapter 6
(Answers appear in Appendix A.)
1. Neurons are treated with a drug that instantly and permanently
stops the Na
+
/K
+
-ATPase pumps. Assume for this question that
the pumps are not electrogenic. What happens to the resting
membrane potential immediately and over time?
2. Extracellular potassium concentration in a person is increased
with no change in intracellular potassium concentration. What
happens to the resting potential and the action potential?
3. A person has received a severe blow to the head but appears to
be all right. Over the next weeks, however, he develops loss of
appetite, thirst, and sexual capacity, but no loss in sensory or
motor function. What part of the brain do you think may have
been damaged?
4. A person is taking a drug that causes, among other things,
dryness of the mouth and speeding of the heart rate but no
impairment of the ability to use the skeletal muscles. What type
Chapter 6 Quantitative and Thought Questions
of receptor does this drug probably block? (Table 6–11 will help
you answer this.)
5. Some cells are treated with a drug that blocks chloride
channels, and the membrane potential of these cells becomes
slightly depolarized (less negative). From these facts, predict
whether the plasma membrane of these cells actively transports
chloride and, if so, in what direction.
6. If the enzyme acetylcholinesterase were blocked with a drug,
what malfunctions would occur in the heart and skeletal
muscle?
7. The compound tetraethylammonium (TEA) blocks the
voltage-gated changes in potassium permeability that occur
during an action potential. After administration of TEA,
what changes would you expect in the action potential? In the
afterhyperpolarization?
Chapter 6 Answers to Physiological Inquiries
Figure 6–12
No. Changing the ECF [K
+
] has a greater effect on
E
K
(and thus the resting membrane potential). This is because
the ratio of external to internal potassium is changed more
when ECF levels go from 5 to 6 mM (a 20 percent increase)
than when ICF levels are lowered from 150 to 149 mM (a
0.7 percent decrease). You can confi
rm this with the Nernst
equation: Inserting typical values, when [K
o
] = 5 mM and
[K
i
] = 150 mM, the calculated value of E
K
= –90.1 mV. If you
change [K
i
] to 149 mM, the calculated value of E
K
= –89.9 mV,
which is not very different. By comparison, changing [K
o
] to 6
mM causes a greater change, with the resulting E
K
= –85.3 mV.
Figure 6–19
The value of the resting potential would change very
little because the permeability of resting membranes to sodium
is very low. However, during an action potential, the membrane
voltage would rise more steeply and reach a more positive
value due to the larger electrochemical gradient for Na
+
entry
through open voltage-gated channels.
Figure 6–22
In all of the neurons, action potentials will
propagate in both directions from the elbow—up the arm
toward the spinal cord and down the arm toward the hand.
Action potentials traveling upward along afferent pathways
will continue through synapses into the CNS to be perceived
as pain, tingling, vibration, and other sensations of the lower
arm. In contrast, action potential signals traveling backward up
motor axons will die out once they reach the cell bodies because
synapses found there are “one way” in the opposite direction.
Figure 6–31
When neuron C alone fi red there would be no
change from the resting membrane potential because increased
chloride conductance would effectively clamp the membrane
potential at that voltage. This is because in a cell with no
chloride pumping, the chloride equilibrium potential and
resting membrane potential have the same value. However, if
A and C simultaneously fi red action potentials, there would be
a depolarization about half as large as that produced when A
alone fi red an action potential.
Figure 6–46
The muscarinic receptor blocker would only inhibit
parasympathetic pathways, where acetylcholine released from
postganglionic neurons binds to muscarinic receptors on target
organs. This would reduce the ability to stimulate “rest-or-
digest” processes while leaving the sympathetic “fi ght-or-fl ight”
response intact. On the other hand, a nicotinic acetylcholine
receptor blocker would inhibit all autonomic control of target
organs because those receptors are found at the ganglion in
both parasympathetic and sympathetic pathways.
9. Which correctly associates a neurotransmitter with one of its
characteristics?
a. Dopamine is a catecholamine synthesized from the amino
acid tyrosine.
b. Glutamate is released by most inhibitory interneurons in the
spinal cord.
c. Serotonin is an endogenous opioid associated with “runner’s
high.”
d. GABA is the neurotransmitter that mediates long-term
potentiation.
e. Neuropeptides are synthesized in the axon terminals of the
neurons that release them.
10. Which of these synapses does not have acetylcholine as its primary
neurotransmitter?
a. synapse of a postganglionic parasympathetic neuron onto a
heart cell
b. synapse of a postganglionic sympathetic neuron onto a smooth
muscle cell
c. synapse of a preganglionic sympathetic neuron onto a
postganglionic neuron
d. synapse of a somatic efferent neuron onto a skeletal muscle cell
e. synapse of a preganglionic sympathetic neuron onto adrenal
medullary cells
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