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BIPN140 2007 MT2 Key

BIPN140 2007 MT2 Key - Cellular Neurobiology BIPN 140...

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Cellular Neurobiology / BIPN 140 Name__ ____ KEY ____________________ SECOND MIDTERM EXAMINATION: KEY Fall, 2007 GENERAL INSTRUCTIONS 1. Please write your name on ALL 7 pages. 2. Please answer each question IN THE SPACE ALLOTTED. 3. For full credit, state your assumptions and show your calculations. 1) _Diane _/10 pts 2) Diane _/10 pts 3) _Cory _/10 pts 4) _Cory __/10 pts 5) _Nicole _/10 pts 6) _Nicole _/10 pts 7) _Yuri /15 pts 8) _Yuri __/10 pts 9) _Peter _/15 pts TOTAL ___________/100 pts 10) ___Peter __/10 pts EXTRA CREDIT (not added into total) WAIVER : By signing this waiver I give permission for this exam to be left for me to pick up in the vestibule by the elevator on the 3rd floor of Pacific Hall. I understand that I may only pick up my own exam. I realize that the Department of Biology and its staff cannot take responsibility for exams, which may be stolen or lost, from this area. If I choose not to sign this waiver, I acknowledge that my exam will only be available for pickup 1:30-2:30 p.m., Monday- Friday from 3140 Pacific Hall. ____________________________________ ______________________________ 1) (10 points) (a) What is the difference between temporal and spatial summation? Which is likely to come into play at neurons in the cortex. Why? 1
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Cellular Neurobiology / BIPN 140 Name__ ____ KEY ____________________ Temporal summation adds PSP depolarizations over time at the same synapse; spatial summation adds PSP depolarizations over space from multiple synapses. Both occur at neurons in the cortex since they receive many synapses from multiple sources. (b) Which at the vertebrate neuromuscular junction? Why? Neither are significant at the NMJ because the muscle fiber receives a single synapse and it always fires suprathreshold (i.e. every EPSP elicits an action potential because it represents 3-fold more ACh release per stimulus than needed!), unless something is seriously amiss. 2) (10 points) What is the metabolism of acetylcholine (ACh), i.e. where and how is it made, destroyed, and remade? (Name the players; don’t need molecular structures.) Acetyl-CoA + choline is converted into ACh + CoA by the enzyme choline acetyltransferase in the presynaptic nerve terminal of cholinergic neurons. The ACh is then packaged into synaptic vesicles, released by exocytosis into the synaptic cleft and degraded into acetate + choline by the enzyme acetylcholinesterase. The choline is recovered into the nerve terminal (by a high affinity choline uptake protein) and re-utilized, along with new acetyl- CoA from mitochondria to produce new ACh. 3) (10 points) (a) What would be the consequences at both the molecular and behavioral level of blocking glutamic acid decarboxylase (GAD) in the brain? Why? Synthesis of GABA would be diminished, the consequence being that inhibitory signaling would be impaired. Behaviorally this would lead to increased excitation and, in the extreme, epileptic seizsures (or fits, etc).
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