C2006/F2402 ’10
Review Questions for Exam #3
Problems 1-5 are from Exam 3 of ’09; problems 6 & 7 are from Exam 3 of ’08. Each exam included a list of
acronyms and abbreviations; these have been omitted to save space.
Botox© is a commercial preparation of Botulinum A toxin. Botox© blocks release of Acetyl Choline (AcCh).
The toxin (inactive) is taken up by endocytosis, activated inside endocytotic vesicles, and released into the
cytoplasm in active form. The active toxin is an endopeptidase which cleaves one of the proteins required for
fusion of vesicles with the plasma membrane.
1. Botox© is used primarily in cosmetic surgery to treat wrinkles caused by aging. Wrinkles can be caused by
changes in the proteins collagen & elastin, loss of body fat, or skeletal muscle.
A-1. Which of the following types of wrinkles will probably be reduced by using Botox©? Wrinkles caused
by (loss of collagen or elastin) (too much collagen or elastin) (overactive muscles) (underactive muscles)
(either type of muscle) (loss of body fat) (none of these) (any of these).
A-2. Botox© is normally injected in very tiny amounts into specific areas. If too much is injected, you
would expect to find (tetanus) (muscle weakness) (both) (one of the other, but can’t predict which) (neither).
Explain both parts of A.
B-1. In order for Botox© to work, the toxin should be injected into (cells) (Inst. Fl. = interstitial fluid)
(either) (both) (neither).
B-2. In order to avoid side effects, Botox© should NOT be injected into (cells) (Inst. Fl.) (blood vessels)
(cells or Inst. Fl.) (blood vessels or Inst. Fl.) (cells or blood vessels) (any of these). Explain both parts of B.
2. For this question, consider synapses at the neuro-muscular junction. (Ignore all other types of synapses.)
When Botox© is used, assume enough Botox© is added to decrease, but not eliminate, the release of AcCh.
A-1. Botox© acts directly on (either pre or post synaptic cells) (both pre and post-synaptic cells)
(presynaptic cells only) (post synaptic cells only) (neither – it only effects events in the synaptic cleft).
A-2. Suppose you add either Botox©, or both Botox© and an inhibitor of acetyl choline esterase, to a
synapse. You then measure muscle twitches when you stimulate the motor neuron. Adding the esterase inhibitor
should (increase) (decrease) (have no effect on) (increase or decrease) the effect of Botox©. Explain A-2.
B. Suppose you have a drug (call it drug C) that blocks the Ca++ channels in the plasma membrane, but not
in internal membranes. You stimulate the motor neuron and measure muscle twitches at the neuro-muscular
junction with and without drug C (no Botox©).
B-1. The primary effect of drug C would be on (muscle) (nerve) (both) (neither) (either one – can’t predict).
B-2. The channels directly affected by drug C should be
(voltage gated) (ligand gated) (neither) (both kinds – some should be voltage gated and some ligand gated).
C. Now suppose you add either Botox© or both Botox© and drug C at the neuro-muscular junction. Then
you stimulate the motor neuron and measure muscle twitches. How would drug C affect the response to
Botox©? The addition of drug C should (increase) (decrease) (have no effect on) (increase or decrease) the
effect of Botox©. Explain how drug C works, and how it effects the response to Botox©.
3. Botox© blocks release of Acetyl Choline (AcCh). For this problem, the mechanistic details are irrelevant.
Botox© has been used successfully to reduce drooling (excessive saliva) by injections at the salivary glands. In
this case, how is Botox© working?
A. In this case, Botox© probably blocks release of AcCh from (muscle) (motor neurons)
(preganglionic neurons of ANS) (postganglionic neurons of ANS) (pre or post ganglionic neurons)
(any of these) (none of these).
B. In this case, Botox© is probably directly affecting (muscle cells) (gland cells) (nerve input from the S)
(nerve input from the somatic system) (nerve input from the PS) (nerve input from either PS or S).
C. The simplest explanation of these results is that drooling is caused by (too much stimulation by PS)
(too much stimulation by S) (lack of stimulation by S) (lack of stimulation by PS) (none of these). Draw the cell
arrangement, show where Botox© acts, and explain C briefly.
C2006/F2402 ’10
Review Questions for Exam #3, cont.
4. People with Horner’s syndrome have droopy eyelids. This can sometimes be corrected by using apraclonidine
eyedrops. Apraclonidine is an alpha2-adrenergic agonist, which causes the superior tarsal muscle (also known as
Müller’s muscle) to contract.
A. These results indicate that ‘Muller’s muscle’ is (smooth muscle) (skeletal muscle) (either one) (neither).
B. Apraclonidine should have approximately the same affect as
(AcCh) (NE) (either one – but can’t predict which) (both) (neither).
C. Without additional information, you can predict that the alpha2-adrenergic receptor is (indirect) (direct)
(neither) (either way). No explanation required for A-C.
D. Muller’s muscle is probably innervated by (the somatic nervous system) (S) (PS) (can’t predict). Circle
all reasonable choices, and explain your reasoning. Explain what effect each part of the PNS would be expected
to have on Muller’s muscle.
E. Suppose the alpha2-adrenergic receptor activates a G protein, and this G protein affects second
messenger levels.
E-1. After the G protein is activated, which of the following should decrease in the cell?
(free calmodulin) (calmodulin bound to Ca++) (free troponin) (troponin bound to Ca++) (length of actin)
(phosphorylated actin) (phosphorylated myosin) (unphosphorylated myosin) (unphosphorylated actin).
(distance between Z lines) Circle all correct choices. Explain on back if you think it is necessary.
E-2. The G protein could work by (activating PLC) (activating AC) (inhibiting AC). Circle all reasonable
choices and explain why each one would or wouldn’t work.
5. Consider the effects of K+ on normal skeletal muscle.
A-1. In normal cells, [K+] inside the cells is (about the same as outside) (lower than outside)
(higher than outside) (depends on the cell type).
A-2. If the [K+] in the ECF is a little higher than normal, the RMP of muscle cells should be
(more negative than usual) (positive, but less so than usual) (negative, but less so than usual)
(neutral – no difference across the membrane) (can’t predict).
A-3. If the [K+] in the ECF is a little higher than normal, the stimulus required to trigger an AP in a skeletal
muscle membrane should be (less than normal) (same as normal) (greater than normal) (can’t predict). Explain
A-2 & A-3.
B. Mutations in the gene for the voltage regulated Na+ channel in skeletal muscle can cause unusual stiffness.
The mutant muscle Na+ channels open (activate) in response to the usual signals, but do not inactivate as rapidly
as normal. (All other channels are normal.) If the muscle Na+ channels are opened (by cold, exercise, or
changes in K+ levels) stiffness results. Patients can make a fist, but cannot open it. These mutations are
dominant, so the patients are heterozygotes, containing both normal and mutant channels.
B-1. While Na+ channels are open, the cell membrane should be (hyperpolarized) (depolarized)
(normally polarized for a cell at rest) (not polarized – no difference across the membrane).
B-2. Stiffness in the patients probably results from (under stimulation from nerve)
(over stimulation from nerve) (low response of muscle) (overactive response of muscle)
(a combination of abnormal neural stimulation plus abnormal muscle response).
B-3. Stiffness results from (too much muscle relaxation) (too much muscle contraction) (either way).
B-4. In stiff muscle, which of the following probably occur? (very high APs) (very rapid APs)
(relatively infrequent APs) (any of these). Explain how the mix of mutant and normal channels could lead to
stiffness. Pin it down as much as you can.
C. Suppose you have samples of some drugs that affect muscle proteins.
C-1. Given your answer to B-3, which drug(s) could you use to relieve the stiffness? You might try out
drugs that activate (MLCK) (tropomyosin binding to Ca++) (ATPase that hydrolyzes soluble ATP)
(opening of Ca++ channels in SR) (release of Ca++ from tropomyosin) (ATP dependent Ca++ pump in the SR
membrane). Circle all correct answers, and explain why ONE of those drugs will work.
C2006/F2402 ’10
Review Questions for Exam #3, cont.
Problem 5, cont.
C-2. Given your answer to B-3, which of the drug(s) should make the stiffness worse? Drugs that activate
(MLCK) (tropomyosin binding to Ca++) (release of Ca++ from tropomyosin) (opening of Ca++ channels in SR)
(ATPase that hydrolyzes soluble ATP) (ATP dependent Ca++ pump in the SR membrane). Circle all correct
answers, and explain why ONE of those drugs will work.
6. AcCh activates skeletal muscle and inhibits cardiac muscle.
A-1. The receptors in the two types of muscle are (both nicotinic) (both muscarinic) (nicotinic in one and
muscarinic in the other) (neither of these).
A-2. The receptors in the two types of muscle are (both cholinergic) (both adrenergic) (adrenergic in one and
cholinergic in the other) (neither of these).
A-3. Heart cells should contain (genes) (mRNA) (both) (neither) for both types of receptors.
No explanation was required on the exam.
B. Both receptors open channels and increase the permeability for K+. However the skeletal muscle
depolarizes and the heart cells hyperpolarize (or depolarize less than normal). Given these results,
B-1. The channels opened by AcCh in the skeletal muscle should allow passage of (K+ and Na+) (K+ only) (K+
or Na+) (K+ and Ca++), AND
B-2. The channels opened by AcCh in the heart cells should allow passage of (K+ and Na+) (K+ only) (K+ or
Na+) (K+ and Ca++). Explain how you get opposite effects in the two cell types.
C. For all of part C circle one or more correct answers for each question.
C-1. Suppose AcCh affects the pacemaker cells in cardiac muscle. In that case, AcCh will change the
properties of the (receptor potential) (pacemaker potential) (action potential) (EPSP) (IPSP) (EPP) (none of
these).
C-2. In the absence of any neurotransmitter, the pacemaker cells have (a steady resting membrane potential)
(no open channels except K+ leak channels) (no APs) (gradual repolarization after each spike) (gradual
depolarization after each spike) (none of these are correct choices for pacemaker cells).
C-3. If AcCh is released onto pacemaker cells, what will happen? AcCh will cause (a change in the height of
the AP) (a change in the width of AP) (a change in intervals between APs) (no more APs) (APs where there
were none before) (a change in something else, but not in APs).
Explain what the expected change is, and how AcCh (and the changes in channel openings) will cause it.
C-4. In the absence of any neurotransmitter, skeletal muscle cells have
(APs that are wider – more prolonged -- than cardiac contractile cells) (a steady resting membrane potential)
(no APs) (none of these are correct choices for skeletal muscle cells). No explanation was required on the exam.
7. You have two neurons with a synapse between them. You drip neurotransmitter on a dendrite of the
presynaptic neuron, and you get an AP in the postsynaptic neuron (if you use enough neurotransmitter).
A-1. In the presynaptic neuron, you probably generated (no APs) (one AP) (multiple APs) (1 or more APs).
A-2. You probably dripped your neurotransmitter on (a bouton) (a glial cell) (a node of Ranvier) (an axon
hillock) (the synapse between the two neurons described above) (none of these).
A-3. In the postsynaptic neuron, you generated (an IPSP) (an EPP) (an EPSP) (an EPSP or IPSP) (a receptor
potential) (none of these).
A-4. Now you drip the same amount of neurotransmitter on the dendrite of the presynaptic neuron in the
presence of lidocaine. Lidocaine is a local anesthetic that binds to and blocks voltage-gated Na+ channels. You
add enough lidocaine to block all the voltage gated Na+ channels.
(a). You would expect to get an AP in the (post synaptic neuron) (presynaptic neuron) (both) (neither).
(b). You would expect to get an EPSP in the (post synaptic neuron) (presynaptic neuron) (both) (neither).
Explain A-4. On exam, no explanation was required for A-1 to A-3.