[Level of delta sleep-inducing peptide (DSIP) in the brain of rats with different alcoholic motivation].
Burov. Iu V IuV; Iukhananov. R Iu RIu; Maĭskiĭ. A I AI
Key Findings
- Short‑sleeping rats show lower DSIP levels in the whole brain, cortex, and striatum.
- A low acute dose of ethanol (1 g/kg) temporarily increases DSIP in the medulla, thalamus, and striatum.
- Higher acute doses (2.5–4.5 g/kg) cause a smaller DSIP rise, and chronic free‑choice alcohol consumption for 12 months reduces DSIP in several brain regions.
Practical Outcomes
- The study suggests alcohol can disrupt the natural balance of a peptide linked to deep sleep, especially with chronic use. For biohackers, it reinforces the idea that regular or heavy drinking may impair sleep quality, but the research offers no direct dosing or supplementation guidance for humans.
Summary
In rats, the amount of a sleep‑related peptide called DSIP changes when they drink alcohol. Short‑sleeping rats naturally have less DSIP in their brains. A single low dose of alcohol briefly raises DSIP in some brain areas, but higher doses and long‑term drinking actually lower it.
Abstract
Radioimmunoassay was used to measure the content of delta-sleep-inducing peptide (DSIP) in random-bred albino rats divided into groups according to the duration of ethanol anesthesia and the levels of 15% ethanol consumption under free-choice conditions. The concentration of the neuropeptide was assayed in intact brain, in the cortex of large hemispheres, medulla oblongata, thalamus and striatum. The short-sleeping rats manifested a statistically significant lowering of the DSIP content in intact brain homogenates, in the cortex of large hemispheres and striatum. On the contrary, thirty minutes after a single intraperitoneal injection of ethanol in a dose of 1 g/kg the DSIP content in the medulla oblongata, thalamus and striatum was found to be increased. The raising of the ethanol dose up to 2.5 and 4.5 g/kg was followed by a less significant increase in the neuropeptide content. Prolonged chronic alcoholization under free-choice conditions led after 12 months to the reduced DSIP content in the medulla oblongata, thalamus and striatum. The importance of DSIP for the pathogenesis of experimental alcoholism using rats with different levels of alcoholic motivation is discussed.
Study Information
pubmed
1982