Psycho-Babble Medication | about biological treatments | Framed
This thread | Show all | Post follow-up | Start new thread | List of forums | Search | FAQ

Re: Any experience with Trintellix?

Posted by linkadge on April 28, 2018, at 9:07:31

In reply to Re: Any experience with Trintellix? linkadge, posted by SLS on April 28, 2018, at 8:18:01

>What are the functions and locations of sigma receptors? I don't know anything about them.

They appear to have neuroprotective and neurotrophic effects. The brain growth factor NGF acts via sigma receptors (just as BDNF acts at trk-b receptors). Sigma agonists appear to have pro-cognitive effects, and can counteract the psychotomimetic effects of NMDA antagonists (or other schizophrenogenic agents). The sigma receptors interact with ion channels (calcium) and also modulate neurotransmitter release. Supposedly combo 5-ht1a + sigma agonists have synergistic effects on cognition.

>What do you think about combining Trintellix >
>with Effexor? Are there any times where
>combining two SRIs is safe? If Trintellix helps >with cognition and memory and Effexor is a
>stronger antidepressant, I may petition my doctor to combine them if Effexor is insufficient.

I'm not sure. I haven't taken trintillex, so I don't have a feel for it. There could certainly be synergy (especially at higher doses of Effexor - which may impact norepinephrine more). Because both bind at the serotonin transporter site, it's possible that the SERT transporter becomes saturated at lower doses of each. If this occurred, each drug would begin to have greater binding at its alternative sites (i.e norepinephrine for Effexor, and 5-ht receptors for trintillex).


>It would be interesting to have my CRP tested.
>Imipramine, desipramine, amitriptyline, and >nortriptyline help me while protriptyline (high >NRI) and reboxetine made me very, very much >worse. Straterra was neutral.

It could be that there are secondary binding sites for the TCAs which exert the anti-inflammatory effects. Wellbutrin supposedly has a strong effect on inflammation - not sure if this is through norepinephrine.

>I would feel uncomfortable doing this. Even at
>6mg/24hr, there is quite a bit of MAO-A
>inhibition. This is acknowledged in the
>manufacturer's label.

I was thinking more oral selegiline. When used in anti-Parkinson doses, it primarily affects MAO-b and can be taken orally. Supposedly, using oral selegiline and SSRIs is not uncommon in parkinsons with depression.

Inhibiting MAO-b (even mildly) can exert a neuroprotective / neurotrophic effect. Also, MAO-b selective doses may have an effect on motivation / anhedonia. MAO-A inhibitors likely do have the stronger effect on traditional depression, however MAO-b inhibitors can still exert a punch on certain depressive symptoms.

>Once I discontinue Parnate, I can try DXM.
>Ketamine was completely inert. I interpret this
>as my probably having the met66met genotype for
>the synthesis of BDNF. This is the worst >
>genotype to have. It's always something with me.

Have you had this tested? If for some reason you do have a bad BDNF gene, there may be hope via direct TRK-b agonists. TRK-b agonists directly activate the 'bdnf' receptors (no BDNF required). Amitriptyline is a trk-b agonist, as are some emerging investigational drugs. The problem with amitriptyline (as you know) is the secondary binding sites. However, there may be more selective trk-b agonists on the way. Sigma receptors also interact with BDNF (although it's a bit too complex for me to understand), however, they can potentiate the action of BDNF at trk-b receptors.

>I began taking Remeron, but aborted it after
>only 2 days because I thought I was feeling a
>worse.

Yeah, I can only tolerate in the 1-2mg range for mirtazapine. The initial antihistamine effects are strong. It may also act as a kappa opioid receptor agonist (which, in the short term, could cause dysphoria).

>I just don't see anyone getting a consistent
>antidepressant effect from it. I do profit from
>Abilify, though. So maybe DA agonism is a good
>thing.

One things BDNF does is sensitize the d3 recpetors in reward regions of the brain. If (for some reason) your BDNF level was low, you could (very theoretically) have recduced dopamine activity at d3 receptors. Mirapex is fairly selective towards d3 (and d2), however it also has some action at 5-ht1a receptors. Another plus is that it exerts neurotrophic / neuroprotective effects. It could be worth a shot (low probability for interaction with other drugs).


Linkadge


Share
Tweet  

Thread

 

Post a new follow-up

Your message only Include above post


Notify the administrators

They will then review this post with the posting guidelines in mind.

To contact them about something other than this post, please use this form instead.

 

Start a new thread

 
Google
dr-bob.org www
Search options and examples
[amazon] for
in

This thread | Show all | Post follow-up | Start new thread | FAQ
Psycho-Babble Medication | Framed

poster:linkadge thread:1098332
URL: http://www.dr-bob.org/babble/20180331/msgs/1098371.html