Selank Inhibits Ethanol-Induced Hyperlocomotion and Manifestation of Behavioral Sensitization in DBA/2 Mice.
Kolik. L G LG; Nadorova. A V AV; Seredenin. S B SB
Key Findings
- Selank (0.3 mg/kg, i.p.) prevented ethanol‑induced hyperlocomotion in DBA/2 mice.
- A single Selank dose blocked the expression of motor sensitization without affecting its formation.
- The effect was comparable to the opioid receptor blocker naloxone, indicating opioid system involvement.
Practical Outcomes
- For biohackers, this hints that Selank might help blunt some of alcohol's stimulating and rewarding effects, but the evidence is limited to mice and requires injection. Until human data are available, it’s not ready for self‑experimentation, though it could inform future research on Selank for alcohol‑related cravings or stress management.
Summary
In a mouse study, the peptide Selank stopped the extra activity that normally shows up after a high dose of alcohol and reduced the development of heightened motor responses to repeated alcohol exposure. It worked similarly to an opioid blocker, suggesting Selank can influence the brain's reward system linked to alcohol.
Abstract
The effect of non-benzodiazepine anxiolytics on the ethanol-induced hyperlocomotion and behavioral sensitization was assessed in male DBA/2 mice. Selank that enhances activity of the endogenous opioid system (0.3 mg/kg, intraperitoneally), similar to the nonselective opiate receptor blocker naloxone (1.0 mg/kg, intraperitoneally), prevented the development of ethanol-induced (2.0 g/kg intraperitoneally) hyperlocomotion, in contrast to σ1-receptors agonist Afobazole (1.0 mg/kg, intraperitoneally) that did not inhibit ethanol-induced behavioral stimulation. Single dose of Selank significantly blocked manifestation of motor sensitization without affecting its formation. These findings suggest that Selank can modulate the motivational effects of ethanol.
Study Information
pubmed
2016
2016-11-23T00:00:00.000Z
10.1007/s10517-016-3544-6