Posted by Quintal on August 15, 2007, at 18:24:05
In reply to Re: Vicodin and Percocet for Depression, posted by linkadge on August 15, 2007, at 13:02:15
>It would have been clearer (for me) that you use the word *can* in your statement. Others may have understood your post completely.
I did use the word 'can' on several occasions but you seemed to persist in finding examples of where I had used sentences without it, sometimes even with in the same post. As I said earlier, by doing this I thought you seemed to be asking for a higher standard of communication than you yourself were willing to provide. You don't have to alter your posting style on my account, but I think it is common courtesy to do so when demanding care and clarity from others.
>You don't have to change the way you post on my account.
Likewise, but it does help ease communication.
>Who says I need to have a purpose.
Do you understand why I might be confused and alarmed by posts that have no apparent purpose? If I have time I will compose a post in reply to one of your questions that has no point, reason, rhyme nor purpose. And does not make sense. How do you think it would feel to be the recipient of such a post?
>Drugs of abuse and antidepressants have destinct and divergent patterns of gene expression (BDNF). Antidepressants increase hippocampal levels of BDNF, but not affecting gene transcription in the neucleus accumbens. Drugs of abuse generally have no positive effect on gene transcription in the hippocampus but tend to increase BDNF in the neucleus accumbens. Enhancing BDNF in the NAA produces a behavioral depressant effect wherase the opposite is true to increasing BDNF in the hippocampus.
Is this linked to the role of BDNF is the mesolimbic dopamine pathway? I see from the first article you provided (and thank you for doing so) that increased BDNF expression in this pathway also produces a behavioral depressant response. Since dopaminergic input from the VTA modulates activity in the NAcc, and does this via the mesolimbic pathway, it would seem that BDNF has an inhibitory role on dopaminergic transmission in the mesolimbic pathway, and thereby the NAcc, which would then produce a behavioral depressant response?
This is slightly confusing because drugs of abuse, like the amphetamine example in the previous post, have been used, and are indeed used, in treatment resistant depression because of their 'mood elevating' effect, which seems quite the opposite of a behavioral depressant response.
>And since you asked, here are, in no particular order, a number of studies pertaining to some of what I have been saying.
Thank you for locating these studies link. I will try to organize them according to topic, assess their relevance, and see what I can glean from them.
>I hope you find some of the above case reports of interest. Listed is one individual who achieved his longest state of clinical remision with a fixed dose of oxcodone. I would assume that a euphoriant effect would not have lasted almost 2 years on a fixed dose. And if it did..all the better!
Yes, achieving the same level of euphoria from a fixed dose of oxycodone taken continuously for two years would be very unusual. It's also possible though, that the level of euphoria did decline over the course of treatment, but that he still felt, and was grateful for, the small relief still provided. I believe a similar thing occurs with long-term benzodiazepine use. For me, after almost one year of continuous use codeine still has some small euphoriant effect, I'd estimate less than 1/10th of what it was in the beginning, yet I still manage better with this small mercy than having no relief at all.
Q
poster:Quintal
thread:775567
URL: http://www.dr-bob.org/babble/20070815/msgs/776487.html