Download Final Exam Practice Problems

Final Exam Practice Problems:
Note: Attempt to do these problems without looking at the book/lectures to make
sure you really know it (you’ll probably want to attempt thema when you’ve done
most of your studying already). Answers will be posted late next week.
1. A ferret embryo is injected with 3H-thymidine at age E29, the age at which new
neurons become layer 6 cells. If the labeled cells are immediately transferred to a
P1 animal (when new neurons end up in layer 2/3), which layer would the labeled
cells go to? If instead of immediately transplanting, you culture the labeled cells
with other E29 cells for 12 hours before transplantation into the P1 animal, what
fate would the labeled cells assume? If instead P1 cells were labeled and
transplanted (immediately) into an E29 embryo, what fate would the cells adopt?
If E29 cells are transplanted to P1 immediately they will adopt the P1 fate (layer 2/3).
If they are cultured for 12 hours first, they will adopt the E29 fate (layer 6), showing
that it is the post-mitotic environment that affects fate. If P1 cells are transplanted to
E29, they will still have the P1 fate (layer 2/3), showing that the progenitors lose
pluripotency.
2. You transplant a sweat gland (which usually receives cholinergic innervation) into
an area of skin that normally receives adrenergic sympathetic innervation. Would
the neurons innervating the transplanted sweat gland be cholinergic or adrenergic?
Cholinergic. This shows that the target is releasing a factor that induces the neurons to
become cholinergic (as opposed to it being dependent on the identity of the neuron).
3. Name three differences between apoptosis and necrotic cell death.
Apoptosis is genetically programmed while necrosis results from trauma or injury.
Apoptosis causes internal degradation while necrosis causes breaking of the cell
membrane and leakage of the cell contents. Apoptosis does not cause an inflammatory
response while necrosis does. [There are other possible answers to this question]
4. Which neurotrophins bind of each of the three Trk receptors?
TrkA=> NGF
TrkB=>BDNF, NT-4/5
TrkC=>NT-3
5. Is there more or less cell death in the ventral cord if a limb is removed from the
embryo? If a limb is added? What does this imply about the relationship between
neurotrophins and survival?
There is more cell death if a limb is removed and less cell death if a limb is added. This
shows that the target synthesizes cell survival factors in limited quantities.
6. In the frog model used by Roger Sperry, what part of the tectum do neurons from
the anterior retina connect to? If the frog eye is detached and rotated 180 degrees,
where will the neurons from the (new) anterior retina go? The guidance to the
neurons’ location in the tectum is governed by interactions between which two
molecules? This is an example of which type of axon guidance?
The anterior retina normally connects to the posterior tectum. When the eye is rotated,
the neurons now in the anterior retina would have originally been in the posterior retina
and will therefore go to the anterior tectum, showing that guidance cues and not
connectivity govern the connections made. This guidance is mediated by interactions
between Eph in the retina and ephrin in the tectum. This is an example of contactmediated inhibition.
7. A growth cone navigating to its destination encounters Netrin released from a
distant target. If the neuron expresses the DCC receptor, will it be attracted or
repulsed by Netrin? If it expresses only DCC and no other receptors, and the
target expresses Netrin and Slit, will it be attracted or repulsed? What if the
growth cone begins expressing Robo?
In the first case, the growth cone will be attracted if it is not expressing the unc-5
receptor, and it will be repulsed if it is expressing unc-5. In the second case, it will be
attracted as the Netrin will have an attractive force (since unc-5 isn’t expressed) and Slit
will have no effect. In the third case, the neuron will be attracted as the Slit/Robo
interaction will cause a strong repulsion that outweighs the Netrin attraction.
8. How does Agrin induce mAChR clustering underneath synapses on muscle
fibers?
Agrin binds to the MuSK receptor, causing another protein, Rapsyn, to bind to multiple
ACh receptors, causing the ACh receptors to cluster together.
9. What is responsible for repressed mAChR expression outside of synapses on
muscle fibers?
Electrical activity (in the absence of AchR activation) causes reduced expression of ACH
receptors. This can be prevented by paralysis.
10. Compare and contrast the sympathetic and parasympathetic divisions of the ANS
with regards to: (1) pre-ganglionic axon length (2) post-ganglionic axon length (3)
pre-ganglionic neurotransmitter (4) post-ganglionic neurotrasmitter (5) metabolic
role (6) location of pre-ganglionic cell body
(1) Symp- short axon; Parasymp- long axon (2) Symp- long axon; Parasymp- short axon
(3) Symp- ACh; Parasymp- ACh (4) Symp- NE; Parasymp- ACh (5) Sympanabolic/active; Parasymp- catabolic/vegetative (6) Symp- chain ganglia or paravertebral
ganglia; Parasymp- distal ganglia close to target organs.
11. What is the hypothalamus composed of, what is it’s primary role?
It is composed of nuclei (clusters of cell bodies). Its primary role is maintaining
homeostasis and modulating behavior (temperature, sleep, hormones, etc.);
12. How does the anterior pituitary differ in function from the posterior pituitary?
Anterior- neurons in the hypothalamus release ‘releasing hormones’ into an intermediate
blood supply that then causes neurons in the anterior pituitary to release hormones into
the main blood supply. Posterior- neurons in the hypothalamus send axons directly to the
pituitary and release hormone into the main blood supply. Also, the anterior and
posterior pituitary release different hormones.
13. What general trend is observable in the EEG of someone going into deeper stages
of non-REM sleep? What are two characteristics unique to stage 2 non-REM
sleep? What differences are observable in the EOG during REM versus nonREM sleep.
The EEG activity tends to become larger amplitude and slower frequency as sleep gets
deeper, going from alpha (8-12 Hz) activity during drowsiness down to delta (0.5-2 Hz)
during stage 4 sleep. Stage 2 is characterized by spindles and K-complexes. During
REM sleep, the EOG is somewhat random and has high amplitude spikes due to sudden
eye movements, while during nREM, if anything, there are only slow rolling motions.
14. If you somehow transplanted the SCN of a human into a mouse, then put the
mouse in a constant light cycle environment, what would you expect to happen to
its sleep cycle?
The mouse’s sleep cycle would get later every day because the human circadian clock has
a period of about 25 hours.
15. What is the biological mechanism by which light entrains the circadian rhythm
(specify either fly or mammal)?
In fly, the protein cryptochrome has a conformational change in response to blue light
which causes it to bind to TIM and prevent it’s degradation (altering the protein cycle
that sets the circadian rhythm. The mechanism is not as well understood in mammals.
16. Name two pieces of evidence that sleep is involved in memory consolidation.
1) If subjects learn a task and then perform it eight hours later, they show better
performance if they slept during the eight hours than if they didn’t. 2) Recordings from
hippocampus show that correlated activity between neurons that occurred during the
learning of a task are replayed during sleep.
17. What brainstem nuclei are involved in the medial descending system? What
tracts do they give rise to? What are the functions mediated by each of these
tracts?
1) The superior colliculus gives rise to the tectospinal tract, which mediates gaze and
keeping the head balanced on the shoulders. 2) The vestibular nucleus gives rise to the
vestibulospinal tract, which is involved in posture and keeping the head balanced. 3) The
reticular formation gives rise to the reticulospinal tract, which mediates antigravity
reflexes.
18. What symptoms would expect to see in someone who has a damaged
corticospinal tract? What is a neurological test that can be used to test for such
damage? Why might babies have a positive result for this test?
Difficulty with coordinated limb movements (e.g., they would pick up an object with
their whole hand instead of their fingers). The Babinski sign is a test for corticospinal
lesions. Babies have a positive Babinski because their corticospinal connections haven’t
fully developed.
19. In the late 1980s, Italian scientists discovered “mirror” neurons. These cells fire
action potentials in response to certain motor movements but additionally will fire
when they see another animal perform the movements, even if the animal they are
being recorded from is totally still (they are believed to be involved with learning
motor skills from other animals). What area of the do you think one might find
mirror?
They are found in premotor cortex. However, Supplementary cortex would probably also
be a reasonable guess.
20. Say you have a sample of four neurons in M1 that are tuned for each of the four
cardinal directions (0, 90, 180, and 270 degrees). An arm movement away from a
central point at a 60 degree angle, what would you expect of the relative firing
rates of the M1 neurons?
The neuron tuned to 90 degrees would fire the most, followed by the neuron tuned to 0
degrees. The other two would not fire as much, though they may still have some activity.
21. Draw a schematic cerebellar circuit with the following elements: the input fibers,
the output, the five types of cells, the deep nuclei, and the connections between
the above (and whether they are excitatory or inhibitory).
22. According to Marr & Albus’ model, learning how to throw darts accurately after
putting on prism glasses would involve what synaptic process at which synapse?
LTD at the parallel fiber – purkinje cell synapse
23. What protein is found in the thick filaments of the muscle fiber? What three
proteins are in the thin filament? Which thin filament protein binds calcium
released from the sarcoplasmic reticulum and what occurs as a result of the
calcium binding?
Thick filaments- myosin, thin filaments- actin, tropomyocin, and troponin. Troponin
binds calcium, which causes a shift in the position of the tropomyosin/tropnin complex in
order to expose myosin-binding sites on the actin.
24. Where are Renshaw cells and what is their function?
They are motor interneurons. They act to modulate contraction to prevent large transient
movements and sensory-motor feedback loops.
25. What are the steps involved in generating movement of the filaments against each
other in order to cause contraction of the muscle fiber?
Initially, the myosin heads are “cocked” and bound to ADP. Calcium binding to troponin
exposes myosin binding sites on the actin, at which point the myosin can bind to the
actin. The myosin heads can now rotate, moving the thin filament relative to the thick
filament and generating the force of muscle contraction (the rotation involves unbinding
of ADP). ATP can now bind to the myosin heads, which is then hydrolyzed to create the
energy needed for the myosin head to go back to its original “cocked” position (the
myosin head is now bound to ADP). At this point the cycle is completed and is ready to
be initiated again.
26. Draw and explain the stretch reflex:
27. Draw and explain the flexion withdrawal reflex: