Effects of delta-sleep-inducing peptide on NMDA-induced convulsive activity in rats.
Shandra. A A AA; Godlevskii. L S LS; Brusentsov. A I AI; Karlyuga. V A VA
Key Findings
- DSIP (100 µg/kg, i.p.) increased the NMDA dose needed to cause clonic convulsions by 2.3‑fold.
- DSIP increased the NMDA dose needed to cause tonic forelimb extension by 4.46‑fold.
- These results suggest DSIP has a neuroprotective effect against excitatory amino‑acid receptor agonists in rats.
Practical Outcomes
- For now, the study is an early animal experiment and doesn’t provide a usable human dosing protocol. It indicates DSIP might help protect the brain from excitotoxic damage, but more research is needed before biohackers can safely apply it for neuroprotection or seizure prevention.
Summary
In rats, giving delta‑sleep‑inducing peptide (DSIP) made the brain much less likely to seize when exposed to a chemical (NMDA) that normally triggers convulsions. The peptide raised the amount of NMDA needed to cause two types of seizures by about 2‑ to 4‑fold, hinting that DSIP could protect nerve cells from over‑excitation.
Abstract
Acute experiments on rats showed that the ED100 of NMDA for induction of clonic convulsions was 0.53 microgram, while the ED100 of NMDA for inducing tonic extension of the forelimbs was 5.02 micrograms/animal. Determination of these parameters after administration of delta-sleep-inducing peptide (100 micrograms/kg, i.p.) revealed 2.3- and 4.46-fold increases. These results provide evidence for a neuroprotective role of delta-sleep-inducing peptide in relation to excitatory amino acid receptor agonists.
Study Information
pubmed
1998
10.1007/bf02462991