[Effects of ethanol on the concentration of neuropeptides, ACTH and corticosterone during immobilization stress].
Iukhananov. R Iu RIu; Rozhanets. V V VV; Maĭskiĭ. A I AI
Key Findings
- Stress raised ACTH, beta‑endorphin, and corticosterone in rats.
- Ethanol (1 g/kg) reduced ACTH but increased beta‑endorphin and DSIP (in the thalamus).
- Immobilization lowered met‑enkephalin in the striatum; ethanol reversed this effect.
Practical Outcomes
- The study hints that alcohol can influence DSIP levels during stress, but it’s an animal experiment with a high ethanol dose. For biohackers, it suggests a possible link between alcohol consumption and DSIP‑mediated stress protection, yet it doesn’t provide a clear, safe protocol for using DSIP or alcohol to improve sleep or stress resilience in humans.
Summary
In stressed rats, alcohol (ethanol) changed hormone and peptide levels: it lowered ACTH, raised beta‑endorphin, and boosted the sleep‑related peptide DSIP in the brain's thalamus. Stress alone didn’t affect DSIP, but alcohol did, suggesting ethanol’s stress‑protective effects might involve DSIP.
Abstract
It was shown, that stress increased the level of ACTH, beta-endorphin and corticosterone in the blood plasma of the rat. Injection of ethanol (1 g/kg) decreased the level of ACTH, but increased the levels of beta-endorphin in the rat subjected to immobilization stress. The immobilization lowered the levels of met-enkephalin in the striatum and medulla oblongata, but increased the content of neuropeptide in the adrenal glands. The concentration of leu-enkephalin and DSIP remained unchanged following the stress. Ethanol reversed the action of immobilization on the level of met-enkephalin in the striatum, but increased the content of DSIP in the thalamus. These results indicate that ethanol modified the activity of pituitary-adrenal-axis during stress and probably the stress-protective action of ethanol partly performed with the involvement of DSIP.
Study Information
pubmed
1989