Assignment
1. Lecture C1
A. Glial cells express and secrete many different proteins, the most abundant of which are the various apo-lipoproteins, lipid carrier proteins. Considering the role of astrocyte cells as neuronal nurse cells, why do you think this is so?
B. A major type of cortical neuron is the pyramidal neuron. Based on what we discussed in class, explain how the shape of this neuronal type serves the primary function of the cortex in integrating information between local as well as distant areas of the brain.
2. Lecture C2,
Astrocytes play a critical role in reducing extracellular glutamate after release from excitatory neurons. Design an experiment to test the fate of glutamate once inside Astrocytes. Is it converted into glutamine and transported to neurons or is it converted into alpha-ketoglutarate and metabolized. Under what circumstances might one pathway predominate?
3. Lecture C3,
You have recently discovered a novel protein you call EndoBender which you hypothesize is involved in regulating rates of syaptic vesicle endocytosis by a mechanism that involves the promotion of membrane curvature.
A. Explain why a protein that promotes membrane curvature would be expected to accelerate rates of synaptic vesicle endocytosis.
B. organism Design an experiment that would test your model that EndoBender promotes membrane curvature. EndoBender is well conserved in evolution, so assume you have the reagents available to study it in any or preparation of interest. Be very specific as to the purpose, design, possible outcome, and conclusion of the experiment.
C. Design three experiments, using complementary approaches, which would allow you to directly evaluate your hypothesis that EndoBender effects rates of synaptic vesicle endocytosis. EndoBender is well conserved in evolution, so assume you have the reagents available to study it in any organism or preparation of interest. Be very specific as to the purpose, design, possible outcome, and conclusion of each experiment.
4. Lecture C4,
Energy demand by neurons leads to increased production of reactive oxygen species by mitochondria. What is an approach could you use to protect neurons against oxidative damage? Include a brief rationale and potential pitfalls in your answer.
5. Lecture C5, *No more than one page for two answers (1 page limit).
A. How do synaptic vesicles, axolemmal precursors and mitochondria move down the axon? Describe the molecular machinery and the "hand-over-hand" mechanism of anterograde axonal transport, and provide one example of an axonal transport defect that is due to damage to an anterograde motor molecule.
B. How do anterograde motor molecules recognize their cargo proteins, for example mitochondria? Describe molecular sorting mechanisms that ensure delivery of mitochondria to specific membrane compartments. How does motor activity stop and then release mitochondria from the motor at the nerve terminal?
6. Lecture C6/C7
A. Describe the historical experiment that led to the first definitive proof of chemical transmission between a neuron and its target.
B. Describe the biogenic amines, their locations of synthesis in the brain and their projection fields. Summarize the predominant functions of each biogenic amine.
C. During the lecture we discussed NO as example for an unconventional neurotransmitter, a gasotransmitter. What properties that define classical neurotransmitters are not describing properties of this NO signaling?
D. In the first publication discussed, what was the key approach that allowed the authors to draw more definitive conclusions than with the studies conducted before? Summarize similarities and differences in how dopaminergic and GABAergic neurons in VTA and serotonergic neurons in dorsal raphe nuclei process reward versus punishment.
E. In the second publication discussed, describe the proposed full life cycle of GABA in nigrostriatal dopaminergic neurons. What is the suggested mechanism of GABA filling into synaptic vesicles and what were the lines of evidence the authors presented to establish this mechanism?