C2006/F2402 ’11
Review Questions for Exam #3
Problems 1-6 = Exam #3 of ’10 (with minor changes noted). Explain all your answers briefly!!
1. The electric organs of fishes are composed of special cells (electrocytes) that discharge currents. See last page
for complete description.
A-1. You would expect to find voltage-gated K+ channels in the electrocytes of electric fish that live in
(salt water) (fresh water) (both) (neither) (can’t predict).
A-2. You would expect to find ungated K+ channels in the electrocytes of electric fish that live in
(salt water) (fresh water) (both) (neither) (can’t predict). Explain both answers.
B. The electric organ of the Torpedo (salt water ray) is a rich source of acetylcholine esterase.
B-1. The esterase should be found in (the electrocyte) (the neuron) (the synaptic cleft) (either cell type)
(any of these).
B-2. If you inhibit the esterase, the shock delivered by the electric ray will probably be (stronger or longer)
(weaker or shorter) (either way – can’t predict).
C. The electric organs form by modification of developing muscle. The muscle fiber and its innervation
develop normally until a late stage and then the muscle changes shape, loses myosin, and becomes an
electrocyte.
C-1. The electrocyte is probably derived from which kind of muscle? (smooth) (cardiac) (skeletal)
(striated – either skeletal or cardiac) (smooth or skeletal) (can’t tell).
C-2. Assume all vertebrates (such as fish and humans) have a similar body plan. Then the cell bodies of the
neurons that innervate the electrocytes in fishes should be (in the CNS) (in a ganglion of the PS)
(in a ganglion of the S) (in either type of ganglion) (can’t predict). Explain how you decided.
2. Suppose an enzyme is normally found in the mitochondrial matrix.
A. The gene for this enzyme was probably transcribed in the (nucleus) (cytoplasm) (mitochondrion)
(nucleus or cytoplasm) (cyto. or mito.) (mito or nucleus) (any one of these).
B. To reach its normal location, the protein would have to pass through (a translocon in the ER)
(a nuclear pore) (the outer mito. membrane = OMM) (the inner mito. membrane = IMM)
(the nucleolar membrane) (a transport vesicle) (the plasma membrane) (an endosome) (a coated pit) (none of
these). Circle all correct answers and explain briefly.
3. Normal mice can detect sweet, sour, bitter, and salty tastes. The receptor cells that detect tastes do not fire
action potentials; when stimulated the cells release NTs onto the dendrites of sensory neurons. The receptor cells
that detect sweetness respond to stimulation by opening the ligand-gated channel TRPM5 (M5). This channel
allows passage of monovalent cations.
A. How should receptor cells in normal mice respond to sweet compounds?
A-1. The plasma membranes in the receptor cells should (depolarize) (hyperpolarize) (either way) (neither).
A-2. Voltage-gated Na+ channels in the receptor cells should (open) (close) (either way) (neither).
A-3. The level of Ca++ in the cytosol of the receptor cells should _______________________
Fill in the blank with increase, decrease, stay the same, can’t predict, or stay the same at zero.
Explain how these events and the opening of the M5 channel are related.
B. Suppose the amount of sweet compound tasted increases, what should happen in the corresponding
sensory neurons?
Fill in the blank with increase, decrease, stay the same, can’t predict, or stay the same at zero.
B-1. In the axon of the neuron, the size of the graded potential should ________________________
B-2. In the axon of the neuron, the interval between spikes should ___________________________
B-3. In the dendrites of the neuron, the size of the graded potential should ________________________
Explain how these events are related.
Problem 3, cont.
C. The taste receptor cells produce many different proteins, including T1R proteins (type 1 taste receptors),
the ligand-gated cation channel TRPM5 (M5), and PLCß2 (a type of PLC). Mice that lack any one of these 3
proteins cannot respond to sweet tastes. Mice lacking these proteins respond normally to sour tastes.
Based on all the information so far about taste reception in mice, how is sweetness detected?
C-1. The receptor proteins for sweetness are probably (ionotropic) (metabotropic) (either way).
C-2. Which of the following proteins probably bind(s) to sweet compounds? (a G protein) (a GPCR)
(PLC ß2) (PKA) (AC) (PKC) (a TF) (the M5 channel) (none of these). Circle all reasonable choices.
C-3. Of the following choices, the M5 channel is most likely to be gated by (a G protein) (Ca++) (cAMP)
(NE) (acetyl choline) (cAMP or Ca++) (can’t predict – any of these are equally likely).
C-4. If sweetness detection uses a 2nd messenger, the 2nd messenger is most likely to be (PKA) (cAMP)
(IP3) (epinephrine) (ATP) (cAMP or ATP) (cAMP or IP3) (cAMP or PKA).
Diagram out or explain how sweetness is detected in receptor cells – how it leads to opening of the M5 channel.
Include the roles of the 3 proteins listed and support your answers. Please work this one out on scratch paper
first.
4. Some recent experiments on taste sensation in mice are described on the last page. Please read and answer
the questions below. Explain all your answers!
A. If the mice are missing the M5 channel, sensory neurons should fire when the mice drink water
containing (Cyx) (sugar) (lemon juice) (sugar or Cyx) (sugar or lemon juice) (lemon juice or Cyx) (any of these)
(none of these).
B. If the mice are missing T1R receptors, they will NOT be able to distinguish (water & sugar solution)
(water & Cyx solution) (either of these) (both of these). Explain briefly.
C-1. The simplest explanation of these results is that the two types of receptor proteins (T1R & T2R) -a. use different signaling pathways in their respective receptor cells.
b. are in cells that synapse on neurons connecting to different cells in the brain.
c. cause their respective receptor cells to release different NTs.
d. are in cells that synapse on the same neurons.
Circle all correct answers.
C-2. Using genetic engineering it is possible to get mice that express T2R proteins only in the cells that
normally express T1R proteins. These mice have no functional T1R proteins. You would expect these mice to:
a. Have a preference for (sugar solution) (Cyx solution) (both) (neither) (can’t predict) AND
b. Have an aversion to (sugar solution) (Cyx solution) (both) (neither) (can’t predict).
Explain your predictions.
Note: Last year, pacemaker cells were covered before exam #3. What you need to know to answer the questions
below is that pacemaker cells fire APs spontaneously. After they fire, they repolarize (as for all APs) and then
the membrane gradually depolarizes (without any stimuli). These cells do not have a stable resting potential –
they spontaneously depolarize. The depolarization is known as the pacemaker potential. Once the membrane
depolarizes to threshold, the pacemaker cells fire again, and so on.
5. The rate of discharges from the electric organs of fish depends on pacemaker neurons. In one kind of electric
fish, the electric organ discharges from females are at higher frequencies (more per sec) than in males. Injections
of an androgen (male steroid) lower discharge frequencies in both sexes. Assume that the steroid affects the
pacemaker cells, not their target cells.
A-1. Then, in the pacemaker neurons of normal fish, which of the following should be higher in females
than in males? (height of action potential) (width of action potential) (number of spikes per min. in axon)
(value of threshold) (value of RMP) (none of these).
A-2. When the steroid is added to female fish, which of the following should increase?
(slope of rising action potential) (slope of pacemaker potential) (slope of falling action potential)
(time for pacemaker potential to reach threshold). Explain A.
B-1. The effect of the steroid should be (immediate) (blocked by inhibitors of transcription).
(blocked by inhibitors of translation) (none of these). For all parts, circle all correct answers and explain briefly.
B-2. The steroid receptor is most likely to be synthesized on ribosomes that are (bound to the ER)
(in mitochondria) (in the cytoplasm) (on ER or in cytoplasm) (in cytoplasm or mito.) (on ER or in mito.)
(any of these). Explain B.
Note: Last year, Question 6 of Exam 3 included some material that has not yet been covered. Those parts of the
question are not included here, and will be included on review questions for the final.
6. The bladder includes three types of muscle – the smooth muscle making up the bladder wall, the smooth
muscle making up the internal sphincter, and the skeletal muscle of the external sphincter. Answer each part and
explain briefly.
C. The sympathetic branch of the ANS causes relaxation of the bladder wall muscle and contraction of the
internal sphincter. The PS has the opposite effect. What should cause relaxation of the bladder wall muscle by
the ANS?
C-1. The pre-sympathetic ganglionic fiber should release (AcCh) (NE) (either one) (neither) AND
C-2. The post-ganglionic fiber should release (AcCh) (NE) (either one) (neither).
D. Consider the synapses on the bladder wall muscle (1) and the synapses on the internal sphincter (2) from the
Sympathetic branch of the ANS.
D-1. The NT(s) at the two types of synapses is/are probably (the same) (different) (can’t predict), AND
D-2. The receptors at the two types of synapses are probably (the same) (different) (can’t predict),
E. What should cause relaxation of the external sphincter? (NE) (AcCH) (either one) (neither).
Problem 7 is from Exam #4 of ’10.
7. See below for a description of a HF and the response.
A-1. In the short run, the response to a HF should cause the core body temperature to (increase) (decrease)
(stay the same) (can’t predict).
A-2. In the short run, the response to a HF should make the face feel (hotter) (cooler) (the same)
(can’t predict).
A-3. After the response to a HF, the core body temperature should (rise) (fall) (stay wherever it is)
(can’t predict).
A-4. The response to a HF is similar to what happens when someone (first starts developing a fever)
(finishes with a fever) (is in the middle of a fever) (is at the start or end of a fever) (beats me).
B-1. The effectors causing the flush -- redness of face -- are (skeletal muscle) (smooth muscle) (liver)
(sweat glands) (pancreas) (red blood cells). Circle all correct choices.
B-2. The regulated variable(s) here is/are (extent of vasoconstriction) (redness of face)
(core body temperature) (face surface temperature) (all of these). Circle all correct choices.
B-3. Consider menopausal women who do or do not have HF episodes. The set point for the regulated
variable should be (higher in women with symptoms) (lower in women with symptoms)
(the same for both types of women) (beats me).
No explanation was required for B on the exam, but you should be able to explain your answers.
C. Estrogen and brain NE affect the frequency of hot flashes. Estrogen decreases them; NE increases them.
Measurements indicate that these substances affect the body’s thermo-neutral zone – defined here as the range
of temperatures that induce neither sweating nor shivering in the body.
C-1. In women who do not have hot flashes, the thermo-neutral zone is about 0.4oC. In these women, the
maximum core body temperature should be about ___________.
C-2. The thermo-neutral zone should be wider in (women without hot flashes) (women with hot flashes)
(either – can’t predict).
C-3. How should NE affect the critical point for sweating? It should (raise) (lower) (have no effect on) the
temperature at which sweating occurs.
C-4. You have two women in a room; one has hot flashes (sometimes) and the other doesn’t. If you cool
down a room, who will probably start shivering first? (The one who doesn’t have hot flashes)
(The one who does have hot flashes) (neither – both will start shivering at the same time) (can’t predict).
On the exam you only had to explain C-4, but you should be able to explain all your answers.
D. The majority opinion is that clonidine, used to treat hot flashes, is an agonist of a presynaptic receptor.
(See last page for details.) In that case,
D-1. Activation of these presynaptic α2-adrenergic receptors should (inhibit NE release)
(stimulate NE release) (inhibit response to NE) (stimulate response to NE) (inhibit NE release or response)
(stimulate NE release or response).
D-2. These receptors could be part of a negative feedback loop. Assume that normal levels of NE do not
have any effect on the presynaptic receptors. Then this feedback loop can be used to correct for
(high NE) (low NE) (both) (neither).
Explain how the feedback loop works, and why someone might think clonidine is an antagonist.
For Problem 1:
Some fishes have electric organs. The electric organs are composed of special cells (electrocytes) that discharge
currents. Electrocytes are usually modified muscle cells that can’t contract but are specialized for discharging
current.
In all marine (salt water) electric fishes, the electrocytes are stimulated by AcCh from neurons. The
membranes of the electrocytes (in marine fishes) generate EPSPs, but no spikes. (There are a lot of electrocytes
connected in series, so the total current can deliver a nasty shock.)
Electrocytes of freshwater fishes have spike-generating membranes.
Electrocytes of both marine and freshwater fishes are innervated in the same way, by cholinergic (nicotinic)
synapses.
For Problem 4.
Normal mice can detect sweet, sour, bitter, and salty tastes.
Normal mice produce T1R (type 1 taste receptors) & T2R proteins (type 2 taste receptors). The T1R proteins are
expressed in one subset of receptor cells and the T2R proteins are expressed in a different subset. Normal mice
show a preference for sweet compounds and an aversion to bitter ones, such as Cyx. If mice are lacking T2R
proteins they can respond to sweet, but not to bitter. If they have no T1R proteins, they respond to bitter, but not
sweet. If they lack the M5 cation channel, or PLC ß2, they don’t respond to either sweet or bitter taste. (They do
respond normally to sour and salty tastes.)
Backgound on hot flashes for Problem 7
Hot flashes (or flushes) are very common in menopausal women. They are triggered by falling levels of
estrogen, but it’s not clear how. (Falling estrogen is necessary, but not sufficient, to trigger them.) During a
‘HF’ episode, the person suddenly feels very hot. In response, she flushes – her face gets red, and she sweats.
The HF only lasts a short time. The average core body temperature of people with hot flashes and those without
is the same – 37oC.
In the past, hormone replacement therapy (with estrogen) was widely prescribed to treat hot flashes. It is
very effective, but has unfortunate side effects. Therefore people are looking for other ways to reduce the
frequency of hot flashes. Two drugs that affect the level of brain NE are clonidine and yohimbine. Clonidine
reduces hot flashes. Yohimbine does the opposite. Both of these drugs affect α2-adrenergic receptors, but it is
not clear exactly how they work. There is disagreement as to whether the receptors are presynaptic or
postsynaptic. There are also some contradictory statements in the literature about whether clonidine is an agonist
or an antagonist.
ABBREVIATIONS
AC = adenyl cyclase
ANS = autonomic nervous system
CNS = central nervous system
EPSP = excitatory post synaptic potential
GPCR = G protein coupled receptor
NE = norepinephrine
PKA = protein kinase A
PLC = phospholipase C
PS = para sympathetic division of the ANS
S = sympathetic division of the ANS
T2R = type 2 taste receptor
TRPM5 or M5 = channel involved in taste
AcCh = acetyl choline
cAMP = cyclic AMP
Cyx = bitter tasting compound (actual name doesn’t matter)
ER = endoplasmic reticulum
IP3 = inositol triphosphate
NT = neurotransmitter
PKC = protein kinase C
PLC ß2 = a type of PLC found in taste receptor cells
RMP = resting membrane potential
T1R = type 1 taste receptor
TF = transcription factor