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Selank

Selanc, TP-7

Quick Stats
Studies 114
Trials 11
Score 2
2006 pubmed 3 citations

Naloxone-blocked depriming effect of anxiolytic selank on apomorphine-induced behavioral manifestations of hyperfunction of dopamine system.

Meshavkin. V K VK; Kost. N V NV; Sokolov. O Yu OY; Zolotarev. Yu A YA; Myasoedov. N F NF; Zozulya. A A AA

Key Findings

  • Selank (0.01‑10 mg/kg, i.p.) reduced apomorphine‑induced hyper‑dopaminergic behavior in mice.
  • The reduction was comparable to low‑dose olanzapine (0.1‑1 mg/kg, i.p.).
  • Naloxone (10 mg/kg, i.p.) blocked selank’s effect, suggesting involvement of the endogenous opioid system.
  • Selank did not displace D2‑dopamine or opioid ligands in receptor binding assays, indicating indirect action.

Practical Outcomes

  • For biohackers, the study suggests selank might influence mood and anxiety by modulating the body’s opioid peptides, not by directly hitting dopamine receptors. However, the work is limited to mouse injections and lacks human safety or dosing data, so it isn’t ready for self‑experimentation or protocol changes yet. It mainly provides a mechanistic clue for future research.

Summary

In mice, the peptide selank lowered dopamine‑related behaviors that are usually triggered by a drug called apomorphine. Its effect was similar to a low dose of the antipsychotic olanzapine and disappeared when the opioid blocker naloxone was given, hinting that selank works through the body’s own opioid system rather than directly binding dopamine or opioid receptors.

Abstract

Peptide 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.

Study Information

Provider

pubmed

Year

2006

Date

2006-11-01T00:00:00.000Z

DOI

10.1007/s10517-006-0428-1

Citations

3

References

12