In its acetylated form, N-Acetyl Selank is a heptapeptide called Selank. The natural tetrapeptide tuftsin (threonine-lysine-proline-arginine) has a synthetic counterpart called Selank. N-Acetyl Selank is made up of the amino acid sequence acetyl-threonine-lysine-proline-arginine-proline-glycine-proline. In the hopes to make it more stable than tuftsin, the C-terminus was modified to include proline, glycine, and proline, while the N-terminus was acetylated. Tuftsin is present in the blood of numerous animals as it is generally situated in the Fc-domain of the heavy link of immunoglobulin G (residues 289-292). This suggests that tuftsin may have immunomodulatory effects.
Studies suggest that neurotransmitters, CNS signaling, and neuroplasticity are all areas where N-acetyl Selank peptide may potentially have an impact. In particular, research suggests that N-acetyl Selank’s potential may reside in improved mental acuity, enhanced serotonin signaling, and increased levels of BDNF. There haven’t been a lot of studies done on N-acetyl Selank, but these findings may be utilized as a point of reference.
N-Acetyl Selank and Cognitive capacity
In a single murine experiment, N-Acetyl Selank’s potential to affect learning, memory, and serotonin levels was studied using trained Wistar rats. The findings implied there may be a 30- to 2-hour window during which N-Acetyl Selank may increase serotonin metabolism in the hypothalamus and caudal brain stem. It’s also possible that N-Acetyl Selank may improve memory trace stability for up to 30 days. These results suggest that N-Acetyl Selank could improve memory storage mechanisms during the last stages of learning. As theorized by researchers, N-acetyl secretagogue may affect serotonin levels and metabolites in the brain, which may account for the compound’s potential to enhance higher cognitive processes.
In addition, the potential of N-Acetyl Selank in isolation was purported in an experimental study by Medvedev et al. (2014). Results from many mood measures, including the HDRS, CGI, Spilberger, and SF-36, were speculated to have improved, prompting academics to hypothesize. It was also said that the “effect lasted for a week after receiving the peptide.”
N-Acetyl Selank and Enkephalins
Enkephalins are neurotransmitters involved in mood and pain perception and are thought to be endogenous ligands for the opioid receptors in the nervous system. Tau(1/2) leu-enkephalin is a metric connected to enkephalin activity in serum, and one experimental investigation proposed that low levels may have anxiogenic potential. N-Acetyl Selank, on the other hand, seems to boost tau(1/2) leu-enkephalin levels without acetylation. It has been hypothesized the peptide may interact with enkephalin transmission in the brain, explaining why it suggested promising results on psychometric scales, including the Hamilton, Zung, and CGI.
In another experimental investigation, a reduction in the half-life of enkephalins and a decrease in total enkephalinase activity were hypothesized to be anxiogenic. It was speculated that N-Acetyl Selank, in its non-acetylated form, may suppress enkephalinase activity, preventing plasma enkephalins from being hydrolyzed by enzymes. The peptide “inhibited enzymatic hydrolysis of plasma enkephalin,” the researchers suggested. Selank appeared to have much higher activity against enkephalinase than the peptidase inhibitors bacitracin and puromycin.
N-Acetyl Selank and Serotonin Signaling
N-Acetyl Selank (NAS) was studied by licensed professionals to see whether it may affect serotonin (5-HT) transmission in the brains of Wistar rats. P-chlorophenyl alanine (PCPA), an inhibitor of 5-HT production, was given to the rats for four days before the experiment. A total of 87 adult rats participated in the research. Researchers proposed that, despite PCPA exposure, the non-acetylated form of N-Acetyl Selank may boost 5-HT metabolism in the brain stem. This data suggests that N-Acetyl Selank, a peptide, could help restore normal functioning when 5-HT metabolism has been impaired.
N-Acetyl Selank and Neurotrophic Growth Factors
The neurotrophic growth factor brain-derived neurotrophic factor (BDNF) has been the subject of much research due to its proposed role in promoting neuroplasticity and synaptogenesis as well as neural remodeling, neurogenesis, nerve cell growth, survival, and adaptability. In addition, researchers suggest, “The neurotrophic factor BDNF is a significant regulator for the growth of brain circuits, for synaptic and neuronal network plasticity, as well as for neuroregeneration and neuroprotection.”
Several studies have examined the potential of N-Acetyl Selank, in both its acetylated and non-acetylated forms, on BDNF expression in the rat hippocampus. Researchers looked at BDNF mRNA and protein levels in particular since this neurotrophic growth factor may play a role in memory formation.
The obtained data purported that N-Acetyl Selank may increase the production of BDNF in the hippocampus, suggesting a possible involvement in regulating hippocampal function. This is because observations hint the rat hippocampus may have exhibited upregulated BDNF mRNA expression in response to the non-acetylated form of N-Acetyl Selank. The introduction of the peptide also seemed to raise the BDNF protein level in the hippocampus.
Conclusion
The possible effects of N-Acetyl Selank on neurotransmitters, CNS signaling, and plasticity have been discussed. It has been hypothesized that by acting on serotonin levels and BDNF expression, N-Acetyl Selank may improve higher cognitive abilities, including memory and learning. In addition, it may have considerable study promise because of its putative connection with enkephalin signaling in the central nervous system.
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References
[i] Semenova TP, Kozlovskiĭ II, Zakharova NM, Kozlovskaia MM. [Experimental optimization of learning and memory processes by selank]. Eksp Klin Farmakol. 2010 Aug;73(8):2-5. Russian. PMID: 20919548.
[ii] Medvedev VE, Tereshchenko ON, Israelian AIu, Chobanu IK, Kost NV, Sokolov OIu, Miasoedov NF. [A comparison of the anxiolytic effect and tolerability of selank and phenazepam in the treatment of anxiety disorders]. Zh Nevrol Psikhiatr Im S S Korsakova. 2014;114(7):17-22. Russian. PMID: 25176261.
[iii] Medvedev VE, Tereshchenko ON, Kost NV, Ter-Israelyan AY, Gushanskaya EV, Chobanu IK, Sokolov OY, Myasoedov NF. [Optimization of the treatment of anxiety disorders with selank]. Zh Nevrol Psikhiatr Im S S Korsakova. 2015;115(6):33-40. Russian. doi: 10.17116/jnevro20151156133-40. PMID: 26356395.
[iv] Zozulia AA, Neznamov GG, Siuniakov TS, Kost NV, Gabaeva MV, Sokolov OIu, Serebriakova EV, Siranchieva OA, Andriushenko AV, Telesheva ES, Siuniakov SA, Smulevich AB, Miasoedov NF, Seredenin SB. [Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia]. Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(4):38-48. Russian. PMID: 18454096.
[v] Zozulya AA, Kost NV, Yu Sokolov O, Gabaeva MV, Grivennikov IA, Andreeva LN, Zolotarev YA, Ivanov SV, Andryushchenko AV, Myasoedov NF, Smulevich AB. The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Bull Exp Biol Med. 2001 Apr;131(4):315-7. doi: 10.1023/a:1017979514274. PMID: 11550013.
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