Selank Reduces Alcohol-Induced Restlessness and Addiction Behaviors in Mice

Alcohol use disorder (AUD) is a complex condition characterized by compulsive alcohol seeking and consumption. Two key behavioral indicators in preclinical models are ethanol-induced hyperlocomotion (increased activity after alcohol) and behavioral sensitization (enhanced response to repeated alcohol exposure), which are thought to model aspects of AUD and craving. While non-benzodiazepine anxiolytics are being explored for their potential in AUD treatment, the specific impact of Selank, a synthetic anxiolytic peptide, on these ethanol-induced behaviors remained unclear.

The study revealed that Selank at 0.3 mg/kg effectively prevented the development of ethanol-induced hyperlocomotion, demonstrating a clear inhibitory effect on this stimulant behavior. This effect was similar to that observed with naloxone at 1.0 mg/kg, suggesting a potential involvement of the endogenous opioid system, which Selank is known to enhance. In stark contrast, the σ1-receptors agonist Afobazole at 1.0 mg/kg did not inhibit ethanol-induced behavioral stimulation, highlighting the specificity of Selank's action and suggesting that its mechanism does not involve σ1-receptors. A single dose of Selank significantly blocked the manifestation of motor sensitization, a key indicator of addiction-like behavior, without affecting the initial formation of this sensitization, indicating its ability to interfere with the expression of learned addictive responses. These findings collectively suggest that Selank can effectively modulate the motivational and behavioral effects of ethanol in a preclinical model.