Cymbalta activating or sedating

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Blocking reuptake means that more ­serotonin is available to get across the synapse to the next nerve cell, or neuron.

Think of it this way: There is a pitcher neuron and a catcher ­neuron. The pitcher can scoop up any balls that aren’t caught immediately with its mitt and throw them again, or just hold on to them.

I have only had a partial remission of my symptoms with this medication.

: "These findings indicate that either the co-administration of an SSRI in addition to a 5-HT3 receptor antagonist or a multimodal agent that acts as a SSRI and 5-HT3 receptor, such as vortioxetine, could enhance 5-HT neurotransmission to produce AD and antiemesis effects, similar to that of litoxetine, after long-term administration." Lecours seems to suggest that augmentation of a classical SSRI to vortioxetine may be a good idea because you have to keep this in mind (also excerpted from the study): "selective 5-HT agents alone, such as escitalopram, and multimodal agents, such as vortioxetine, alter 5-HT neurotransmission through different receptors and exert different actions, via transporter and/or receptor activity, on the serotonergic system in the hippocampus consistent with other antidepressant strategies and with a unique pharmacological profile." Supplementary, compared to other SSRIs, this study revealed: "vortioxetine has a low occupancy for the 5-HTT, escitalopram was used at a dose of 5 mg/kg in order to better mimic the effects of low occupancy alone." I'm suggesting, based upon these excerpts that I've provided from Lecours' study, that augmentation of a traditional SSRI would perhaps enhance vortioxetine's unique pharmacological effects for patients that are diagnosed with MDD? It's also possible that vortioxetine's unique mechanism of action lowers the occupancy requirement so that increased SERT blockage won't give any more benefit, just more side effects.

which is a study by Maurice Lecours who works at the University of Ottawa, Institute of Mental Health Research. I am actually on Day 41 of my Brintellix (vortioxetine) prescription; however, for the past 12 days, I have been administering 20mg. I'm not so sure if I'd follow the suggestion of my own thread title, but I was wondering what everybody thought about the following excerpts paralleled to patients like myself that have not responded adequately to vortioxetine monotherapy for MDD? In general SSRI's need around 70-80% SERT occupancy to achieve therapeutic effects (see for a review), so increasing occupancy could have an additive effect.

If you block the pitcher’s mitt, there are more ­serotonin balls available to eventually be scooped up by the catcher’s mitt.

This blockage results in enhanced serotonin getting across to the catcher.

Add a 50-100mg trazodone at night for insomnia and enhanced 5HT response if necessary.

All three of these drugs cost less than \month, which is probably less even once combined than Brintellix, and Lamictal XR 250mg Lexapro 20mg Trazodone 50mg can all be taken in one handful at night. I'm also prescribed Dexedrine IR, Provigil and Xanax XR.

This is referred to as increased serotonergic tone.

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