[Effect of leu-enkephalin and the delta-sleep-inducing peptide, M (DSIP), on endogenous noradrenaline release by brain synaptosomes in the rat].
Rozhanets. V V VV; Anosov. A K AK
Key Findings
- Leuâenkephalin reduced depolarizationâinduced noradrenaline release, an effect blocked by naloxone.
- Deltaâsleepâinducing peptide (DSIP) showed no impact on noradrenaline release at concentrations from 10â»âž to 10â»â”âŻM.
- A synthetic aminoâacid mixture mimicking DSIPâs composition altered spontaneous noradrenaline release.
Practical Outcomes
- For biohackers, this study suggests DSIP is unlikely to directly boost brain noradrenaline levels, so it offers no clear dosing or protocol benefit. The findings are mainly mechanistic and not ready for realâworld application.
Summary
In a lab test on rat brain particles, the peptide DSIP did not change the amount of the stressârelated chemical noradrenaline that was released, while a related opioid peptide did. Only a mix of amino acids that looks like DSIPâs building blocks had a small effect on the baseline release.
Abstract
Fluorometry was employed to measure the noradrenaline (NA) content in rat brain synaptosomes depending on the duration of incubation, depolarization effects (40 mM KCl or 1.5 mM ouabain), composition of the synaptosomal fraction and concentration of the peptides. The 10-minute incubation in a potassium medium of a suspension of light synaptosomes was used as an optimal test-system for studying the peptide action. Leu-enkephalin inhibited the depolarization-induced NA release. The effect was abolished by naloxone. The delta-sleep-inducing peptide (DSIP) did not influence the neurotransmitter release at concentrations of 10(-8)-10(-5) M. A mixture of amino acids imitating the amino acid composition of the DSIP influenced spontaneous release of NA. This effect is discussed in connection with the physiological action of the peptide on its intraventricular injection.
Study Information
pubmed
1985