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onedayillsailagain

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Posts posted by onedayillsailagain

  1. Well to each their own opinion. I still believe that progress involves taking risks.
    That said; I've quit NSI-189 due to lack of efficacy, although that may have been due to several factors, one of which is that I've only taken it for no longer than 3 weeks.
    Also; the group buy on Longecity seems to have fallen through.. The organizer got scammed. I got a refund, but I'd suggest for anyone not to join until it is sorted out.

  2. HDAC2 inhibitors.. I knew of one but can't remember which it is.. I'll try to look it up. Was it C16 maybe? Or was it GEBR-7B? One of those maybe.
    For PTSD-esque fear extinction I'd say NMDA agonism as well as neurogenesis a la 7,8-DHF. I'm kind of low on funds right now, but I'll be trying 7,8-DHF soon as I can afford it.

  3. Good to hear from you Ghormeh; hope you're doing good.

    Unfortunately, one of the participants backed out last-minute. -sad face- sick of waiting.
    So looks like the buy is open to participants until the 6th of February.
    With some luck, I'll have it next month somewhere, and hopefully the JDTic sooner to pull me through until then.

  4. Just posting to say that there's a GLYX-13 buy going on.. We've only got 4 people so far, but that's enough to buy.
    If you wanna join, visit Longecity or shoot me a PM ('formergenius' @ LC).
    We're hoping to finalize before Wednesday, otherwise we have to wait for Chinese New Year to pass. Sorry for the short notice.
    It's $250/g excl. shipping and 3rd party analysis; a bit on the expensive side, but I'd thought I'd inform you guys anyway.
    There's only 4 grams available; but I'm sure one of the participants wouldn't mind splitting a gram so as to make the purchase cheaper.
    It could be that we don't finalize before said deadline, in which case new participants will have until the 6th of February to join.

  5. Nice comprehensive post syntheso!
     

     

    These effects were accompanied by reduced intracortical inhibition and increased expression of brain-derived neurotrophic factor in the visual cortex

    Increased BDNF is good, but I'm not so sure about intracortical disinhibition.. seems to be exactly what perpetuates HPPD in the first place.
    Maybe the 5HT2C antagonism is in part responsible for these effects.. But you've tried 5HT2C antagonists to no avail, right?

    This article may be interesting by the way. Perhaps TrkA agonism is involved? Seems to be NGF mediated..
    This may also be of interest.
    And a bunch of interesting articles

  6. I disagree. There's no evidence to indicate it is toxic or dangerous so far.

    Russian roulette is taking a random party pill or that funny looking blotter from the street dealer.
    Though I haven't had this batch tested; I'll give you that.
    I rather damage myself trying to find something that helps, than never trying at all.
    It's a personal assessment people need to make for themselves; whether the potential benefit is greater than the risk.

    Anyway, ~2 weeks in and unfortunately I haven't seen any benefits. Going to up my dose to 40mg BID today and take it from there.
    I am, however, much more excited about JDTic and GLYX-13/NRX-1074, and the a7nAChR agonists, in that they're more likely to give results quicker, whereas it is in my understanding that NSI-189 may take a while to take effect. My second batch of NSI-189 should be arriving somewhere soon though.

  7. Basically that means that when stress/anxiety worsens your symptoms, it appears this is not mediated via the 5HT2A/C receptors.
    I found this pretty interesting; it implies our deficits in sensory gating are not mediated by these receptors that were initially believed to be the culprit (in inducing HPPD at least). Does seem less and less that 5HT is involved with the 'persistent' part of it all. Or so I take out of this. Unless of course CRF antagonizes 2A/C receptors in the first place..

     

     

    These findings suggest that CRF does not decrease PPI via effects on 5-HT, since neither blockade of 5-HT(2A/C) receptors nor 5-HT depletion attenuated this decrease.

    http://www.ncbi.nlm.nih.gov/pubmed/18280562

    • Upvote 1
  8. Was looking for more info to try and gauge to what extent JDTic might influence symptoms, and came across this.
     

     

    These findings confirm the role of the dynorphinergic system in mediating the effects of drugs of abuse, such as 3,4-methylenedioxy-N-methylamphetamine, in various regions of the rat brain, which may be important sites for the opioidergic mechanisms activated by addictive drugs.

    http://www.mdma.net/opioidergic/prodynorphin.html

    • Upvote 1


  9. "from the start of the day
    to the end of the race
    we thought we had this all figured out
    without a moment to waste
    but we choke, we choke on our words
    we waste all of our days
    throw off another year
    living our lives is our greatest fear

    from being useless to being used
    we lie awake wondering why another year is wasted
    another chance to live PASSED BY US
    this on the tip of our tongues
    the silence of our lives
    but this flame keeps burning
    we'll never lay down and die

    this isn't hopeless
    we'll keep on fighting until the bitter end
    this isn't hopeless
    we'll carry on

    forget about the boundaries
    we'll leave the past behind
    with every step we take
    we'll finally redefine
    WE'LL CARRY ON

    we are the bright lights
    let's not stop shining
    this life will always be worth living

    from the start of the day
    to the end of the race
    we thought we had this all figured out
    without a moment to waste
    WE'LL HAVE OUR WAY"
    • Upvote 1
  10. With recent investigations into a7nAChR agonists and PAMs for their potential therapeutic value as nootropics in cognitive disorders such as Schizophrenia and Alzheimer's, I thought they might pose an interesting new candidate for experimental evaluation in HPPD.

    As such, I've been looking for a link between drugs of abuse, HPPD, and these receptors.
    Here's an excerpt of what I've found:

     

     

    A recent study of our group has demonstrated a direct interaction of MDMA with alpha-7 nicotinic receptors and that this drug induces their up-regulation as nicotinic ligands do. We also have demonstrated that, in rats, the serotonergic injury induced by MDMA is alpha7 nicotinic receptor-dependent.
     

     
    Though they do pose Memantine to be a preventative treatment:
     

     

    Therefore, we can hypothesize that MEM, preventing MDMA-induced neuronal injury, contributes to ameliorate cognitive impairment produced by MDMA, and both glutamic acid and alpha7 receptor antagonism are responsible of this beneficial effect.

    Presuming that this pretreatment is to limit excitotoxicity (NMDAR antagonism) as well as antagonism the a7nAChRs to limit aforementioned serotonergic injury, Memantine really isn't my focus though; taking it would be controversial anyways.

    What it does point out is that during MDMA exposure, there's - as we know - excitotoxicity, but also apparently a7nAChR dependent serotonergic injury as a result of agonism. Hence, what does that say about HPPD? To be honest I've not read this with much scrutiny, but this does raise questions to what the extent of the involvement is of these receptors, and how they may be implicated in the pathogenesis, sustenance, and more importantly amelioration of HPPD. Note that these receptors have also been implicated in a number of substances of abuse, such as cocaine and marijuana.

     

    Again; I don't know to what extent and how they may be implicated, but they do seem to be in some way.
    In any case, you can download the PDF here.

     

    You can find more about a7nAChR agonists here.
     

    • Upvote 2
  11. Ahh intersting indeed Though decreasing neuroinflammation has done nothing for me personally alas.. Perhaps curcumin (LongVida; most bioavailable brand) isn't potent enough though.

    As for your article, if you post a request in /r/scholar, there's a kind fella over there who can get you it.

    As for NMDA; keep an eye out for developments on NRX-1074. Soon as the structure is known, you can expect a group buy for it.
    Also, as a side note; serotonergic injury of MDMA is alpha7nAChR-dependent. More about that later; trying to work on that, but it does interact with cholinergic systems.
    You might be interested in my recent Reddit post; covers new candidates to look out for.

    Given your success with LLLT, I'd suggest you try tDCS if you haven't already. And I'm just gonna assume you're also going to try NSI-189?
    Anyways; thanks for sharing.
    Cheers!

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