Use of Selank to correct measures of integrative brain activity and biogenic amine levels in adult rats resulting from antenatal hypoxia.
Semenova. T P TP; Kozlovskaya. M M MM; Zuikov. A V AV; Kozlovskii. I I II; Zakharova. N M NM; Andreeva. L A LA
Key Findings
- Selank (300 µg/kg, i.p.) increased sensory attention by 2‑3 times in rats with prenatal hypoxia
- Learning speed improved by about 1.5 times after Selank treatment
- Serotonin and noradrenaline levels were restored to normal, balancing brain monoamine activity
Practical Outcomes
- Selank shows promise for reversing brain deficits caused by early‑life oxygen loss, but the evidence is limited to rodents and uses an injection dose that isn’t directly translatable to humans. Biohackers should view this as early‑stage research; more human safety and dosing studies are needed before practical use.
Summary
In a rat study, giving the peptide Selank after birth helped fix brain chemistry and boost attention and learning that were damaged by low oxygen during pregnancy. The drug balanced serotonin and norepinephrine levels and made the animals behave more normally in tests of curiosity and focus.
Abstract
The effects of Selank, the active component of which is the heptapeptide Thr-Lys-Pro-Arg-Pro-Gly-Pro, which includes the tetrapeptide tuftsin and three natural levorotatory amino acids, on behavior and brain serotonin and noradrenaline levels were studied in adult rats subjected to antenatal hypoxia on days 14-16 of gestation. Administration of Selank (300 microg/kg, i.p.) improved sensory attention levels by factors of 2-3 (p < 0.01), facilitated the learning process by a factor of 1.5 (p < 0.01), normalized the level of investigative activity in the open field and hole board, and restored the balance of activity between the serotoninergic and noradrenergic systems of the brain. The data obtained here provide evidence that Selank can be used to compensate for the long-term negative effects of antenatal hypoxia on brain integrative activity and the activity of monoaminergic transmitter systems.
Study Information
pubmed
2008
2008-02-01T00:00:00.000Z
10.1007/s11055-008-0030-2
6
21