Study summary · research use only
Naloxone-blocked depriming effect of anxiolytic selank on apomorphine-induced behavioral manifestations of hyperfunction of dopamine system
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this mouse and rat study, the peptide anxiolytic selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) was given intraperitoneally to mice at doses of 0.01, 0.1, 1.0, and 10.0 mg/kg, and the authors report it reduced apomorphine-induced behavioral manifestations in the verticalization test. This response was described as comparable to the antipsychotic olanzapine (0.1 and 1.0 mg/kg) and was blocked by the opioid antagonist naloxone (10 mg/kg). Radioreceptor assays on rat brain membranes showed selank did not displace the D2 antagonist 3H-spiperone (EC50 >100 microM) or the opioid ligand 3H-DADLE (EC50 >40 microM) from binding sites. The authors hypothesize the behavioral response is mediated by modulation of the endogenous opioid system, specifically enkephalin-degrading enzymes.
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.
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