Diminished Neural Processing of Aversive and Rewarding Stimuli During Selective Serotonin Reuptake I
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Luis Fernando Lopez
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Re: Diminished Neural Processing of Aversive and Rewarding Stimuli During Selective Serotonin Reupta
interesting find! although the title by itself says nothing new: its kind of common knowledge that ssri are fundamentally blunting and blah-inducing!
some excerpts i found particularly interesting:
"reboxetine did not suppress ventral striatal activity and in fact increased neural responses within medial orbitofrontal cortex to reward."
reboxetine is way under trialed! i like how it works but unfortunately it makes my penis shrink totally. i have not really seen many other people reporting about that issue so maybe its just me. would be interesting to hear others experiences in the field of pssd.
it might be possible to improve the efficacy of SSRIs through the recruitment of pharmacologic mechanisms that enhance neural responses to reward as well as diminishing responses to aversive stimuli.
A straightforward way to achieve this could be the use of serotonin and noradrenaline reuptake inhibitors (SNRIs) such as duloxetine and venlafaxine.
there have been a few reports (on this board and elsewhere) of pssd getting much better or even disappearing after using small doses of snri and phasing in and out. I myself have been contemplating this for a while, and venlafaxine seems like the most activating choice from what ive been reading. although people at normal therapeutic range do complain about erectile issues. (safe spots being super low or super high due to DA inhibition)
edit:
just found this, which contradicts me totally and is quite disheartening:
Differential physiological effects of a low dose and high doses of venlafaxine in major depression.
https://www.ncbi.nlm.nih.gov/pubmed/16690006
The present data showed that, at its minimal effective dose in depression (75 mg/d), venlafaxine acted as a selective 5-HT reuptake inhibitor, whereas when administered at higher doses (225 and 375 mg/d), it acted as a dual 5-HT and NE reuptake inhibitor.
although i dont really think 75mg is a low dose
(also i have no idea if the methods they used to assess the levels are precise)
some excerpts i found particularly interesting:
"reboxetine did not suppress ventral striatal activity and in fact increased neural responses within medial orbitofrontal cortex to reward."
reboxetine is way under trialed! i like how it works but unfortunately it makes my penis shrink totally. i have not really seen many other people reporting about that issue so maybe its just me. would be interesting to hear others experiences in the field of pssd.
it might be possible to improve the efficacy of SSRIs through the recruitment of pharmacologic mechanisms that enhance neural responses to reward as well as diminishing responses to aversive stimuli.
A straightforward way to achieve this could be the use of serotonin and noradrenaline reuptake inhibitors (SNRIs) such as duloxetine and venlafaxine.
there have been a few reports (on this board and elsewhere) of pssd getting much better or even disappearing after using small doses of snri and phasing in and out. I myself have been contemplating this for a while, and venlafaxine seems like the most activating choice from what ive been reading. although people at normal therapeutic range do complain about erectile issues. (safe spots being super low or super high due to DA inhibition)
edit:
just found this, which contradicts me totally and is quite disheartening:
Differential physiological effects of a low dose and high doses of venlafaxine in major depression.
https://www.ncbi.nlm.nih.gov/pubmed/16690006
The present data showed that, at its minimal effective dose in depression (75 mg/d), venlafaxine acted as a selective 5-HT reuptake inhibitor, whereas when administered at higher doses (225 and 375 mg/d), it acted as a dual 5-HT and NE reuptake inhibitor.
although i dont really think 75mg is a low dose
(also i have no idea if the methods they used to assess the levels are precise)
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