LEC 28

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LEC 28
2015-11-23 11:42:12
lec28 lec 28 neuro

Lecture 28 neuro
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  1. Body temperature
    • High during the day
    • Low at night
  2. Potassium excretion
    • Excretion of waste
    • High during the day
    • Low at night
  3. Plasma cortisol
    • Jump when you wake up, helps you get going
    • From adrenal glands
    • Decreases throughout the day
  4. Growth hormone
    • High when you sleep
    • Low during the day
  5. Purpose of Kleitman and Richardson’s cave experiment?
    • 33 day experiment
    • Determined whether the human body-clock can be adjusted
  6. What are the features of circadian rhythms?
    • Period of 24 hours is roughly maintained
    • Rhythm persists in absence of external cues
    • Can be entrained with light
    • Rhythm maintained over a range of temperatures (body tem controlled by metabolism)
  7. What is a common feature throughout phylogeny?
    • Circadian rhythms
    • Bacteria colony growth
    • Opening/closing of mimosa leaves
    • Diurnal and nocturnal animals
  8. How does a protein synthesis inhibitor affect the rhythm of the clock?
    • Inhibitor stops clock
    • Different from covering clock
    • Remove inhibitor and clock starts again from where it left off
  9. What is the key molecular component for the clock?
    “Period” gene
  10. What happens when there is a mutation in the period gene per locus?
    Arrhythmic activity
  11. What causes arrhythmic activity?
    A mutation in the “period” gene per locus
  12. What does SCN stand for?
    Suprachiasmatic Nucleus
  13. Where is the SCN located?
    • Hypothalamus
    • Neuroendocrine center
    • Sits right above optic chiasm
  14. What is an optic chiasm?
    Where optic nerves/RGC cross
  15. What is the SCN?
    • Suprachiasmatic Nucleus
    • Master circadian clock in mammals
  16. What kind of input does the SCN receive? From where?
    • a. Axon projections
    • b. Retina
  17. Why does the SCN receive input from the retina?
    Want clock to be entrainable by visible input coming in
  18. How do we know the SCN is necessary?
    • Lesion/knock it out, lose normal activity rhythms; prevents entrainment
    • Transplant it back, regains consistent rhythm, though augmented
  19. How do we know the SCN is sufficient?
    • Lack of it = arrhythmic activity
    • Presence (even from a donor) = restore rhythmicity
    • Cultured brain slices containing SCN maintained rhythmicity
    • Isolated SCN neurons also maintain rhythmicity
  20. What happens over time with isolated SCN neurons?
    • Go out of sync with one another
    • Individual neurons express their own rhythms
    • Don’t communicate with other cells
  21. How can we visually see activity in the brain?
    • Using GFP (fluorescent signal)
    • Glows green during the day, breaks down with rhythm
  22. What drives the expression of GFP in the SCN?
    The promoter for Per 1
  23. Is the SCN the only cell type that has circadian clocks?
    • No, lots of cells express clock/rhythm
    • But not important for driving behavior
    • Ex. Liver and kidney work at diff times
  24. How is the clock entrained by light?
    From intrinsically photosensitive Retinal Ganglion Cells (IpRGCs)
  25. What does IpRGC stand for?
    Intrinsically photosensitive Retinal Ganglion Cells
  26. What happens when we remove eyes?
    Rhythm is gone
  27. How do we know it’s not just the rods and cones telling us about light in the environment?
    If we remove them, can still entrain circadian rhythms to light
  28. How do we know that it’s the Retinal Ganglion Cells (RGCs) that respond to light?
    • Inject fluorescent beads into retina that label the SCN
    • Or inject “retro-beads” into the SCN that dyes/labels some RGCs (opposite direction)
    • Even after synapses are blocked w/ an antagonist, they continue to respond to light
    • Therefore, signal isn’t from photoreceptor cells. They’re from RGCs themselves
  29. How do IpRGCs respond to light?
    Using melanopsin
  30. What is melanopsin?
    Protein similar to rhodopsin
  31. What happens when the melanopsin gene/protein is knocked out?
    RGCs lose their light-sensitivity
  32. What are PER and TIM?
    Proteins named Period and Timeless
  33. When are PER and TIM transcribed and translated?
    Early morning and throughout afternoon
  34. What happens to PER and TIM during the evening time?
    • There is enough protein that they start to create heterodimers in the cytoplasm
    • PER/TIM
  35. How does the heterodimer PER/TIM affect the creation of individual PER and TIM proteins?
    • Negatively regulates their creation
    • Moves to the nucleus and shuts down their transcription
  36. How is the repression of PER/TIM stopped?
    • Blue light activates photoreceptor cryptochrome (CRY), which is associated with TIM
    • Regulates TIM’s degradation
    • Stops repression and allows more transcription of individual PER and TIM proteins
    • Restarts cycle
  37. What must be done to fully stop entrainment?
    Triple knockout
  38. What 3 things must be knocked out to fully stop entrainment?
    • Transducin alpha-subunit (rods)
    • CNG channels (cones)
    • Melanopsin (IpRGC)