Hip
Senior Member
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I always seem to find your posts about a new thing to try right when I am considering trying it.
I guess that might be the result of me being a forum old timer!
I always seem to find your posts about a new thing to try right when I am considering trying it.
@Hip did you get any benefit from tianeptine?
I seen no reaction from it either way
I guess that might be the result of me being a forum old timer!
How does the pricing compare to the nootropics sites that offer it. My mom is using it for her depression and I want to help her find a long term affordable sourcrIf you are looking for pharmaceutical tianeptine, most of the prescription-free pharmacies listed in this post stock it.
How does the pricing compare to the nootropics sites that offer it. My mom is using it for her depression and I want to help her find a long term affordable sourcr
Psychiatrist in what country prescribed it?So after 6 or so weeks using legit tianeptine prescribed by my psychiatrist, I can report I feel zero difference in my anxiety, sensory issues, stress tolerance.. well, no difference in anything.
Psychiatrist in what country prescribed it?
Background
Autism spectrum disorder (ASD) is associated with deficits in executive functioning (EF), and these have been suggested to contribute to core as well as co-occurring psychiatric symptoms. The biological basis of these deficits is unknown but may include the serotonergic system, which is involved both in regulating EF in neurotypical populations and in the pathophysiology of ASD.
We previously demonstrated that reducing serotonin by acute tryptophan depletion (ATD) shifts differences in brain function during performance of EF tasks towards control levels.
However, ATD cannot be easily used in the clinic, and we therefore need to adopt alternative approaches to challenge the serotonin system. Hence, we investigated the role of the serotonergic modulator tianeptine on EF networks in ASD.
Method
We conducted a pharmacological magnetic resonance imaging study, using a randomized double-blind crossover design, to compare the effect of an acute dosage of 12.5 mg tianeptine and placebo on brain activation during two EF tasks (of response inhibition and sustained attention) in 38 adult males: 19 with ASD and 19 matched controls.
Results
Under placebo, compared to controls, individuals with ASD had atypical brain activation in response inhibition regions including the inferior frontal cortex, premotor regions and cerebellum.
During sustained attention, individuals with ASD had decreased brain activation in the right middle temporal cortex, right cuneus and left precuneus.
Most of the case–control differences in brain function observed under placebo conditions were abolished by tianeptine administration.
Also, within ASD individuals, brain functional differences were shifted significantly towards control levels during response inhibition in the inferior frontal and premotor cortices.
Limitations
We conducted a pilot study using a single dose of tianeptine, and therefore, we cannot comment on long-term outcome.
Conclusions
Our findings provide the first evidence that tianeptine can shift atypical brain activation during EF in adults with ASD towards control levels.
Future studies should investigate whether this shift in the biology of ASD is maintained after prolonged treatment with tianeptine and whether it improves clinical symptoms.
Tianeptine was initially considered to be a selective serotonin reuptake enhancer (SSRE) as its acute and long-term administration decreased extracellular 5-HT levels in the brain stem, striatum, cerebral cortex and hippocampus in rats [22, 23].
Later studies, however, contradicted these findings—albeit this discrepancy may be explained by technical differences in the micro-dialysis techniques employed.
Nevertheless, recent evidence in humans demonstrates a reduction in plasma serotonin and increase in platelet serotonin following acute administration of tianeptine, consistent with the effect of enhanced serotonin reuptake [50].
In addition, tianeptine has also been shown to: (1) regulate stress-induced glutamate release, (2) modulate plasticity in the amygdala; (3) reverse stress-induced hippocampal dystrophy [51]; and (4) be a μ-opioid receptor agonist [52].
Given that we only investigated the brain response after a single dose of tianeptine, it is unlikely that our results are due to modulating plasticity or the reversal of dystrophy.
However, we cannot rule out the possibility that our results may be partially explained by modulation of the glutamatergic and μ-opioid systems. For example, the glutamatergic system has been widely reported to be abnormal in ASD [53].
Also, alterations in the μ-opioid system have been proposed to contribute to ASD [54]. Hence, future studies are required to investigate which of the proposed mechanisms underlie the reported modulating effect.