Actual Last Email: Papers!

To simplify the paper pick-up process I have left all of the term papers in a box outside of 46-4152 (the locked equipment hallway). You can come get them any time! Don't forget to take both your rough and final drafts!

There are very few comments on the final drafts. If you'd like more feedback feel free to contact me!

Happy Holidays!!!
Julie

(If i told you previously to find me in lab, ignore that -- the papers are now in the hallway!)

Announced on 14 December 2005  12:03  p.m. by Julie Goldberg

Last email hopefully -- 2 suggestions and general exam info recap

Hi Class,

1) Go to bed before midnight so that your memory can be consolidated during sleep.
2) When you have reviewed the material, if you have time, please go to "Discussion" of the class website and read through the questions and answers that I posted under "exam 2". This can help you test yourself how much you understand. Of course the list is not a comprehensive one, but it can serve as the last minute checklist.

3) For undergrad: 75 fill in the blank answers
For grad: 81 fill in the blanks and 1 essay question

Best of luck! See you tomorrow.
TAs

Announced on 05 December 2005  8:59  p.m. by Show Ming Kwok

Propranolol and PTSD

Why is propranolol given to people after they've had trauma to help prevent PTSD? I have PTSD as an anxiety disorder, related mostly to GABA...? But propranolol blocks NE Beta receptors... what is the link?

I don't know why they decided to give the patients propranolol and what is the link between NE betaR and PTSD... Maybe this is an example of existing drug that happens to have a novel effect on other diseasse. Anxiety is related to GABA though.
But this is the result of a pilot study I can find.

Propranolol may be considered for treatment of post-event hyperarousal. One study suggests that treatment with a beta-adrenergic blocker following an acute psychologically traumatic event may reduce subsequent posttraumatic stress disorder (PTSD) symptoms (Pitman et al., 2002). Within 6 hours of a traumatic event patients were randomized to a 10-day course of propranolol (n = 18) versus placebo (n = 23) 40 mg four times daily. The mean (SD) 1-month Clinician-Administered PTSD Scale (CAPS) score of 11 propranolol completers was 27.6 (15.7) compared to 20 placebo completer’s average score of 35.5 (21.5) (t = 1.1, df = 29, p = 0.15). Two propranolol-treated patients' scores fell above, and nine below, the placebo group's median (p = 0.03,sign test). None of the eight propranolol-, but six of 14 placebo-treated patients were physiologic responders during script-driven imagery of the traumatic event when tested 3 months afterward (p = 0.04, one-tailed t-test). These pilot results suggest that acute, post-trauma propranolol may have a preventive effect on subsequent PTSD.

Announced on 05 December 2005  8:55  p.m. by Show Ming Kwok

General info about the exam

I've talked to a few people about this, and we are all a little confused. I understand that the exam tomorrow is cumulative. Is it cumulative in the sense that Dr. Wurtman will ask us detailed questions from the first half of the semester that have not been built on in the second half (for example, a question about PKU or the affinities of different aa's to albumin), or do you mean that we just need to understand the basic concepts from the first half to understand the second half's material (for example, understanding how PLC cleaves phosphatidyl ethanolamine)?

The bottomline is that you should not be surprised if he asks you a NT that we discussed in the first half of the class. So, you do need to know the details of the first half in the relevant content of the second. For example, he can ask you any NTs and drugs from the first half and compare their action to the NTs and drugs that we covered in the second half. You need to know both.....

Announced on 05 December 2005  8:47  p.m. by Show Ming Kwok

Correction about Gi

If the Gi protein decreases cAMP, doesn't it
INACTIVATE adenylyl cyclase (AC)? Also, by activating PLC, doesn't it INCREASE the Ca++ level because PLC activates the release of Ca++ from intracellular stores?

Yes, you are right. There was a typo in my previous email. It should INACTIVATE AC.
What Dr. Wurtman was saying in class is that the more immediate effect of Qi activation is that Ca++ decreaes first. But then after the initial decrease, after a short delay, Ca++ can increase. He did not mention the effect of PLC in that particular lecture. So for example DAG's downsteram effect was not mentioned and Ca++ induced Ca++ release was not taught in this class (<-you really don't have to know for this exam). I added in there just to elucidate the effect of PKC. The time courses of the two Ca++ are different. The internally released Ca++ is slower since GPCR-G-protein-PKC - DAG,IP3-IP3 receptor-Ca++ release is a much longer pathway than inactivating Ca++ channels.
If during the exam the question is not clear, ask one of us.

Recap:
Gs: increase cAMP, activate AC, Ca++ channel activation
Gi: desrease cAMP, inactivate AC, Ca++ channel inactivation and decrease Ca++ level, activate PLC
Gq: activate PLC

Announced on 05 December 2005  6:18  p.m. by Show Ming Kwok