Updated Selank Trial

by admin on January 23, 2012

After my initial success with the Russian Nootropic, Selank, I have decided to do a little experiment (You can read about my initial response to Selank here). Most of the information I have gathered from around the internet suggests a dose of 1-3mg per day. I have been using about 250-500 micrograms of it. Perhaps the higher dosages are because the main route of administration for Selank seemed to be intranasally in the form of a nose spray. It would seem to me, some of the potency would be lost with this method and so injectable forms might prove to be as beneficial, while needing less than normal amounts for the same intended effect. Nevertheless, I’m an adventurer, so what the hell.

I ordered 5 more bottles from here and plan on running 2mg per day for ten days to see what, if anything, arises from this increased dosage. I am splitting the dose up in two injections – late afternoon and early evening. I just recently took my last 1mg injection about twenty minutes ago. I’m struggling to stay awake at this point. Now, let me explain that I did get up rather early this morning so I’m due to feel some fatigue today. There seems to be another level to this fatigue though. Not a knockout feeling, but a subdued and relaxed feeling, urging me to curl up on the couch and let the dog snuggle up next to me as I sleep off the next hour or so.

In general though, sleepiness has not been a common effect for me on this. The effect has been much more qualified as a mood stabilizing effect. I suppose I’m feeling sleepy because I’m tired, I just ate two apples with peanut butter, and I took something that activates, or degrades the enzymes responsible for breaking down endorphins.

You see, one of the the studies I pulled up about Selank mentions that Naloxone, a potent opiate receptor blocker reversed Selank’s ability to make mice get jazzed on apomorphine (Something I’d love to get a hold of one of these days anyways). So it seems we have one mechanism involved with Selank, the ability to modulate our own internal opiate system.

Naloxone-blocked depriming effect of anxiolytic selank on apomorphine-induced behavioral manifestations of hyperfunction of dopamine system.
Meshavkin VK, Kost NV, Sokolov OY, Zolotarev YA, Myasoedov NF, Zozulya AA.
SourceResearch Center of Mental Health, Russian Academy of Medical Sciences, Moscow. meshavkin@ rcmh.msk.ru
AbstractPeptide anxiolytic selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) applied intraperitoneally in doses of 0.01, 0.1, 1.0, and 10.0 mg/kg to mice reduces behavioral manifestations of dopaminergic system induced by apomorphine in the verticalization test. This effect was comparable to that of atypical antipsychotic olanzapine in near-therapeutic doses (0.1 and 1.0 mg/kg, intraperitoneally) and was blocked with nonselective opioid receptor antagonist naloxone (10 mg/kg, intraperitoneally). Radioreceptor assay showed that selank did not displace nonselective D2-dopamine receptor antagonist (3)H-spiperone (EC50>100 microM) and delta- and micro-opioid receptor ligand 3H-DADLE (EC50>40 microM) from specific binding sites on rat brain membranes. It is hypothesized that the revealed behavioral effect of selank is mediated by its modulating effect on the endogenous opioid system and specifically, by its effect on activity of enkephalin-degrading enzymes.

I found another interesting study here that points out mice that are given a drug that halts serotonin production in the brain were given Selank, and that Selank reversed this inhibition. Perhaps that’s why I’m feeling noddy. Extra serotonin following an indulgent snack during the afternoon =  sleepy time.

[Comparison of the effects of selank and tuftsin on the metabolism of serotonin in the brain of rats pretreated with PCPA].
[Article in Russian]
Semenova TP, kozlovskiĭ II, Zakharova NM, Kozlovskaia MM.
AbstractEffects of the peptide drugs selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) and tuftsin (Thr-Lys-Pro-Arg) on the metabolism of serotonin (5-hydroxytryptamine, 5-HT) in the brain of Wistar rats preliminarily treated with the 5-HT-synthesis inhibitor p-chlorophenylalanine (PCPA, 320 mg/kg, i.p., 4 days before experiment) have been studied on a group of 87 matured rats. It is established that selank enhances the 5-HT metabolism in the brain stem 30 min after injection to animals pretreated with PCPA. In contrast to selank, tuftsin induced no changes in the 5-HT metabolism in the brain stem and decreased it in the neocortex on the same time scale. The data obtained suggest that the peptide drug selank can be used for the correction of disturbances induced by a decrease in 5-HT metabolism.

Another interesting facet of Selank is that it has anti-viral properties. You see, Selank is an analog of a naturally occurring peptide called tuftsin. Tuftsin is strung together like this Thr-Lys-Pro-Arg, which means a Threonine amino acid is attached to a Lysine which is attached to a Proline which attaches to Arginine. Selank is the same peptide, except for the addition of a Pro-Gly-Pro, or Proline, Glycine Proline.  In mice studies exploring the immune system, scientists have discovered a Proline-Glycine peptide has a pronounced effect on cytokines, chemokines and their respective receptors. If you notice, this almost a near match at the end of the Selank, which is Pro-Gly-Pro. Scientists discovered Selank shares some of this other peptide’s abilities to modulate inflammation signals.

[Comparison of the effects of selank and tuftsin on the metabolism of serotonin in the brain of rats pretreated with PCPA].
[Article in Russian]
Semenova TP, kozlovskiĭ II, Zakharova NM, Kozlovskaia MM.
AbstractEffects of the peptide drugs selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) and tuftsin (Thr-Lys-Pro-Arg) on the metabolism of serotonin (5-hydroxytryptamine, 5-HT) in the brain of Wistar rats preliminarily treated with the 5-HT-synthesis inhibitor p-chlorophenylalanine (PCPA, 320 mg/kg, i.p., 4 days before experiment) have been studied on a group of 87 matured rats. It is established that selank enhances the 5-HT metabolism in the brain stem 30 min after injection to animals pretreated with PCPA. In contrast to selank, tuftsin induced no changes in the 5-HT metabolism in the brain stem and decreased it in the neocortex on the same time scale. The data obtained suggest that the peptide drug selank can be used for the correction of disturbances induced by a decrease in 5-HT metabolism.

Last but not least I’d like to mention anhedonia. That’s a state of blahness. You simply get no pleasure out of things anymore. Maybe you’re not depressed, hell maybe you are pretty content with life. But nothing pushes your button. Eating seems like a chore, sex just doesn’t get your attention anymore and maybe a favorite hobby of yours has gone unnoticed for a while because it just doesn’t lead to satisfaction. That’s what I say when people ask me what anhedonia is. As a matter of fact, I first explain that this is how I feel, and then I give it the fancy name. I struggle with this issue, if you can call it that.

So what I found so interesting about the research in Selank is that scientists are looking at ways to detect anhedonia in rats. In addition to depression tests, like the forced swimming test (don’t ask), they have added a sucrose taste test in an attempt to measure whether or not the mouse is feeling anhedonic. If the mouse is pretty jazzed, then he will continue to self administer the sucrose. If he just doesn’t get any kicks, then he won’t keep pushing the button. Selank seemed to help restore the hedonic tone of the mice, as more of them continued to self administer the sucrose.

[Effects of heptapeptide selank on genetically-based and situation-provoked symptoms of depression in behavior in WAG/Rij and Wistar rats, and in BALB/c mice].
[Article in Russian]
Sarkisova KIu, Kozlovskiĭ II, Kozlovskaia MM.
AbstractA synthetic derivative of the endogenous peptide tuftsin heptapeptide selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) possesses an anxiolytic and psychostimulant effect, and represents a working element of a new peptide drug having completed the third phase of the clinical testing as a selective anxiolytic. The neurobiochemical spectrum of selank action combines mechanisms which are characteristics of antidepressants and psychostimulants: activation of the brain monoaminergic systems, dopamine synthesis and turnover, and modulation of the tyrosine hydroxylase activity. The aim of this study was to investigate the effect of selank in a new model of inherited (genetically-based) symptoms of depression in behavior of inbred WAG/Rij rats in comparison with its effect on situation-provoked symptoms of depression in behavior of BALB/c mice. Outbred Wistar rats constituted control group. Selank in high doses (1000-2000 microg/kg), after repeated injection counteracted symptoms of depression in behavior of WAG/Rij rats (increased immobilization in the forced swimming test and decreased sucrose intake or preference (anhedonia)). Selank in low doses (100 and 300 microg/kg) after single injection reduced the duration of immobility of BALB/c mice in the forced swimming test, but did not exert significant effect after repeated injection or after injection in high doses (600 and 900 microg/kg). Selank did not affect the level of general locomotor activity and anxiety in WAG/Rij rats, and did not exert substantial effect on the behavior of control Wistar rats. The results demonstrate the presence of antidepressant component in the spectrum of neuropsychotrophyc activity of selank and indicate the higher reliability of a new experimental model of depression (the WAG/Rij rats) as compared to the standard forced swimming test for the determination of antidepressant activity of a pharmacological drug.

So at this point here’s what I know.

  • Selank is based off Tuftsin, an immune peptide produced by the spleen.
  • Selank increases endorphins, most likely via an inhibition of the enzymes that normally keep endorphins in check.
  • Selank restores serotonin metabolism in spite of measures to inhibit it.
  • Selank is immunomodulatory, meaning it has an effect on cytokines, chemokines and their receptors.
  • Selank increases Tyrosine Hydroxylase, which is a rate-limiting step in the production of Dopamine in the brain.

I will write in once more about my trial of 2mg by the end of the week. If things continue at this rate, I may have to buy up as much as I can before it’s run out of stock, or before the “man” decides I don’t know what’s good for me.

 

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