Delta-sleep-inducing peptide stimulates melatonin, 5-methoxytryptophol and serotonin secretion from perifused rat pineal glands.
Ouichou. A A; Zitouni. M M; Raynaud. F F; Simonneaux. V V; Gharib. A A; Pévet. P P
Key Findings
- DSIP directly stimulates the release of melatonin, 5‑methoxytryptophol, and serotonin from isolated rat pineal glands.
- The melatonin‑boosting effect of DSIP is dose‑dependent (effective between 5 µM and 100 µM) and occurs faster but for a shorter duration than isoproterenol.
- Blocking beta‑adrenergic, alpha‑1‑adrenergic, or opioid receptors does not stop DSIP’s effect, suggesting a novel, non‑adrenergic mechanism.
Practical Outcomes
- For biohackers, DSIP may act as a natural way to raise melatonin and serotonin levels, potentially supporting sleep and mood. However, the effective concentrations in this rat study are much higher than typical supplement doses, and human relevance is unproven, so any protocol should be experimental and cautious.
Summary
The study shows that the peptide delta‑sleep‑inducing peptide (DSIP) can make rat pineal glands release more melatonin, a sleep hormone, as well as serotonin and a related compound. This effect happens at fairly high concentrations, works faster than the classic stimulant isoproterenol, and doesn’t rely on the usual adrenaline or opioid pathways.
Abstract
The pineal gland is known to synthesize numerous indolamines. Since delta-sleep-inducing peptide (DSIP, a tryptophan nonapeptide) is found in the pineal gland, its effect on the secretion of indolamines was investigated. DSIP stimulated melatonin (MEL), 5-methoxytryptophol (5-ML) and serotonin (5-HT) synthesis and release, whereas it did not affect pineal cyclic AMP levels. The stimulatory effect of DSIP on MEL secretion was dose dependent between 5 x 10(-6) and 10(-4) M, whereas the minimal effective concentration of DSIP on 5-ML secretion was higher than 10(-5) M. The effect of DSIP (10(-4) M) was compared to the effect of isoproterenol (ISO, 10(-6) M) on MEL and 5-HT release. ISO stimulated MEL secretion and concomitantly decreased 5-HT release. With regard to kinetic characteristics, the effect of DSIP (10(-4) M) on MEL release was faster and of shorter duration than the effect of ISO (10(-6) M; 2 and 4 h, respectively). At 10(-4) M, DSIP potentiated the ISO-induced increase of MEL secretion. The DSIP-stimulated release of MEL was not significantly altered when the pineal glands were treated with 10(-5) M propranolol (a beta-adrenergic antagonist), 10(-5) M prazosin (an alpha 1-adrenergic antagonist) or 10(-5) M naloxone (an opioidergic antagonist). This study demonstrates that the DSIP-induced secretion of indolamines from rat pineal glands may not be elicited through the well-known noradrenergic or opioid systems.
Study Information
pubmed
1992
1992-03-01T00:00:00.000Z
10.1159/000109312
14