MCDB 3650 Take Home Quiz 2: 50 Pts. Due by Monday 12/16 at 5 Pm

MCDB 3650 Take Home Quiz 2: 50 pts. Due by Monday 12/16 at 5 pm

(Note—I extended the time to complete the take home so that it is no longer due at the time of the scheduled final, but rather the following Monday).

Please put your name at the top of this document AND in the name of the file if you send the quiz to me by email.

1. a. (4) Explain how the basal ganglia functions, in general, to regulate movement, and how deficits can lead to either excessive movement or lack of movement.

b. (4) Anne had early onset Parkinson’s in the early 1990s. A then new drug, Requip, a dopamine agonist, was given to her to control the typical symptoms of Parkinson’s. A few months after Anne started taking Requip, she went to Vegas with some friends and discovered she liked playing the slot machines. Suddenly, she was hooked. She became a seriously compulsive gambler, playing the slots almost 24 hours a day, and over a few year period, lost about $300,000. She wanted to stop, but couldn’t. One day, her neurologist got wind of what had happened, and suggested she stop taking Requip. Within a few weeks, she was completely cured. Explain the brain areas and pathways involved that connect a Parkinson’s treatment to addictive behavior. How are addictions are reinforced, what are the long-term changes in the brain that result from addiction? What are some possible differences between an addiction like gambling and an addiction to an actual drug?

2. (7) Using evidence from readings and in-class discussions, discuss the different regions of the brain that are known to contain mirror neurons, and describe how these mirror neurons are thought to work. How are mirror neurons connected to empathy, and how are these systems, or dysfunction of these systems related to autism and the salience landscape theory? What evidence exists to support the idea that there is a connection between mirror neurons and empathy?

3. (8) Explain how the phenomena of priming and condition (including habituation and sensitization) are connected to long term potentiation and ultimately, memory. What is known about the molecular basis of memory from other organisms, and how we have extrapolated these findings to understanding memory in humans. What is the evidence that memories are encoded and stored in different areas, and how do retrograde and anterograde amnesia differ? Why can amnesiacs remember how to do certain things (ride a bicycle, play an instrument) but not remember who somebody is?

4. (7) How are music and language similar? How are they different? Use evidence described in class and in the readings to explain the brain regions involved processing and create these related expressions of human culture. What evidence supports or does not support the idea that perception of music is “innate”, and what is the evidence that our brains are flexible with regards to processing sound, thus impacting both language and music production and perception?

5. (6) One of the explanations for synesthesia includes physical changes in wiring the brain that could allow for something to be “seen” in response to hearing it—i.e., seeing the color red when a note is played on the piano. How might this experience be dependent on how the brain is “wired”, and how could this be affected (or not) by plasticity? How might synesthesia be connected to the evolution of language? 6. (7) Describe the impact of hormones on brain development, and further, their role in brain function. What brain regions are affected by the release of hormones like oxytocin and seretonin, and how do such hormones affect behavior? What seems to be stronger in terms of behavioral outcome, environmental conditions (stress, bonding, etc), or genetics ?

7. (7) In the experiment shown, 10 subjects learned two tasks: the pairing of geometrical figures and a mirror tracing task. Then, they were given (during sleep) stimulation to increase their slow wave sleep, or a sham stimulus. They were tested for recall of figures over baseline and drawing time. What do the results (and other we studied in class) suggest about slow wave sleep, and why is it different from REM sleep? What is one theory of the role of the molecular chaperone BiP in the process of brain cell “health”, and how might this be connected to sleep?