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BISC 407: STUDY GUIDE MATERIAL FOR MODULE 1 Exam II 1. What are iPS cells (3)? o

Induced pluripotent stem cells. A combination of 4 transcription factors expressed in a differentiated adult cell can “reprogram” the cell to become pluripotent; capable of differentiating into a variety of cell types.

2. During neuromuscular junction synapse elimination, there are ______ in immature muscle, while _______ is observed at mature muscle (2): A. Multiple neurons innervating multiple muscles, multiple neurons innervating single muscles B. Single neurons innervating multiple muscles, single neurons innervating single muscles C. Multiple neurons innervating single muscles, single neurons innervating single muscles D. Multiple neurons innervating multiple muscles, single neurons innervating multiple muscles E. Single neurons innervating multiple muscles, multiple neurons innervating single muscles 3. Define the four classes of diseases that affect the motor unit (4)? o

Motor neuron disease; peripheral neuropathy; NMJ disease; myopathy

4. The active zone is an electron dense region at presynaptic terminals that coordinate synaptic vesicle exocytosis. 4.A: Describe the “T-bar” structure often observed at active zones. (1)? o An electron dense structure that resembles a “T” localized at the center of the

active zone (1). 4.B: Discuss how our understanding of Bruchpilot (BRP), the scaffold that makes up the T-bar, changed with super resolution (STED) imaging (2)? o

STED imaging revealed BRP puncta were actually “doughnuts” instead of dots. At the center of the BRP doughnut, Voltage-gated calcium channels were found to exist (2).

5. Active zones are sites of synaptic vesicle fusion at presynaptic terminals. Given your knowledge of the factors and structures that coordinate vesicle release at active zones, define three primary factors that influence the efficacy and/or probability of synaptic vesicle fusion at active zones (3)? o

The amount of calcium influx, the number of synaptic vesicles available for release, the localization of SVs near calcium influx (3).

6. Name and describe the functions of the three major types of muscle (3)?

o

Smooth muscle (internal movements, e.g. bloodflow); cardiac muscle (pumping blood); skeletal muscle (moving bones) (3)

7. What three aspects of movement can neurological disorders impact (3)? o Action potential conduction along motor nerve; synaptic transmission at NMJ;

muscle contraction itself (3) 8. A patient walks into your office (you are an MD), and complains of poor muscle tone, lethargy, reduced EMG responses after repeated stimulation, and weak muscles, including “droopy eyelids”. What is your preliminary diagnosis, given what you’ve learned in this class? (2): o Myesthenia gravis (2). 9. What type of drug would you prescribe to improve symptoms of this disease? (you don’t need to state the name of the drug, just what it does/targets) (3): o

Acetylcholinesterase inhibitor (3)

10. From all that you have learned in this course, define what you think is the best explanation for the function of sleep (3)? o To homeostatically adjust synaptic strength 11. What are the 2 areas of adult brain where neurogenesis occurs (3)? o

Subventricular zone (SVZ) of the dentate gyrus and the olfactory bulb (3)

12. What are the two routes that synaptic vesicles take after endocytosis to replenish the SV pool (3)? o

Direct trafficking back to the SV pool and through endosomal intermediates (+1.5 for each; 3)

13. Define the 3 mechanisms proposed for SV endocytosis and the conditions in which they are thought to operate (6). o

Kiss-and-run: Low intensity stimulation; 2) Clatherin-mediated: normal physiology; 3) Bulk endocytosis: periods of chronic, intensity stimulation (6)

14. Discuss the role of molecular codes and activity in synaptogenesis (3)? o

Molecules (cell adhesion proteins, axon guidance factors) typically define the general process of axon guidance, target recognition, and synaptogenesis. Activity is dispensable for these major steps, but help to refine the final pattern (involved in pruning away or stabilizing synapses

15. What is fatal familial insomnia (3)? An autosomal dominant genetic disease that leads to progressive neurodegeneration of key sleep promoting centers of the hypothalamus. Mutations in a gene that confers a “prion-like” protein misfolding is thought to be involved (3)....