Effects of Selank on behavioral reactions and activities of plasma enkephalin-degrading enzymes in mice with different phenotypes of emotional and stress reactions
Sokolov OYu, Meshavkin VK, Kost NV, Zozulya AA
Bulletin of Experimental Biology and Medicine (2002)
The bridge between Kost 2001 in vitro mechanism and Zozulya 2008 clinical biomarker: in BALB/c mice (high anxiety phenotype), 100 µg/kg Selank produced an anxiolytic effect and prolonged plasma leu-enkephalin half-life; in C57BL/6 mice (low anxiety phenotype), it did neither. Strain-dependent responsivity consistent with an opioidergic mechanism.
The in vivo bridge between the Kost 2001 in vitro mechanism paper and the Zozulya 2008 clinical biomarker finding. The Sokolov / Kost / Zozulya group compared two inbred mouse strains with opposite anxiety / stress phenotypes — BALB/c (high baseline anxiety) and C57BL/6 (low baseline anxiety) — for their responsiveness to Selank in two paired read-outs: open-field behaviour and plasma leu-enkephalin half-life.
Baseline plasma leu-enkephalin t½ already differed between strains. In BALB/c mice, a single 100 µg/kg dose of Selank produced an anxiolytic effect in the open field and prolonged plasma leu-enkephalin half-life. In C57BL/6 mice, the same dose had no detectable effect on either behaviour or enkephalinase activity.
The authors interpret the result as confirming, in vivo, the Kost 2001 hypothesis that Selank's anxiolytic activity is mediated by inhibition of enkephalin-degrading enzymes — and as additionally showing that the magnitude of that response depends on the baseline state of the enkephalinergic system: animals with already-fast enkephalin turnover and high anxiety are responsive; animals with slower baseline turnover and low anxiety are not.
The published abstract reports the direction of effect but does not enumerate specific half-life values, sample sizes per group, or per-trial open-field parameters. The 100 µg/kg dose tested is a single dose point, not a dose-response curve. The strain-dependent responsiveness pattern is consistent with multiple alternative mechanisms beyond pure enkephalinergic ones (differential receptor expression, brain peptide penetration, HPA tone).
Single-group result; the strain-dependent pattern was however replicated and extended by Kozlovskii et al. 2012 (PMID 22550852) using naloxone pretreatment to show that the opioid antagonist reduces Selank responsiveness in BALB/c and increases it in C57BL/6 — consistent with the opioidergic interpretation. Abstract-only extraction.
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