Phosphorylated delta sleep inducing peptide restores spatial memory and p-CREB expression by improving sleep architecture at high altitude.
Roy. Koustav K; Chauhan. Garima G; Kumari. Punita P; Wadhwa. Meetu M; Alam. Shahnawaz S; Ray. Koushik K; Panjwani. Usha U; Kishore. Krishna K
Key Findings
- p‑DSIP (10 µg/kg, i.p.) increased non‑REM and REM sleep during chronic hypobaric hypoxia in rats.
- Improved sleep was associated with better performance in the Morris water maze, indicating restored spatial memory.
- p‑DSIP raised hippocampal p‑CREB levels, a molecular marker of memory consolidation, and altered brain monoamine enzyme expression.
Practical Outcomes
- For biohackers, the study suggests that DSIP‑related peptides might help protect sleep quality and memory under stressful low‑oxygen or high‑altitude conditions, but the evidence is limited to rodent models and injectable dosing. Until human trials are available, any self‑experimentation would be speculative and should consider safety, delivery method, and regulatory issues.
Summary
In rats exposed to simulated high‑altitude low‑oxygen conditions, daily injections of a phosphorylated form of delta sleep‑inducing peptide (p‑DSIP) improved both deep and REM sleep, which in turn helped the animals perform better on a water‑maze memory test. The peptide also boosted a brain protein (p‑CREB) linked to memory formation. However, the work was done only in animals, using an injection dose that isn’t directly translatable to humans.
Abstract
Sleep loss at high altitude (HA) play major role in worsening of neuropsychological functions, such as attention, memory and decision making. This study investigates the role of phosphorylated delta sleep inducing peptide (p-DSIP) in improving sleep architecture during chronic hypobaric hypoxia (HH) exposure and restoration of spatial navigational memory. Morris water maze (MWM) trained rats were exposed to HH at 7620 m. p-DSIP was injected intra-peritoneally (10 μg/Kg bw) during HH exposure as an intervention against sleep alteration. Sleep architecture was recorded telemetrically before and during HH exposure. Monoamines were estimated by high performance liquid chromatography from brain stem (BS) and hypothalamus. CREB and p-CREB level in hippocampus was studied by western blotting and expression of different monoamine regulatory enzymes in BS was measured by flow cytometry. Naloxone (1 mg/kg bw), a μ opioid receptor antagonist of sleep inducing effect of DSIP was also studied. p-DSIP injection daily in circadian active period (18.30 h) during chronic HH enhanced non rapid eye movement sleep, rapid eye movement sleep as well as improved MWM performance of rats. p-DSIP treatment showed lower monoamine level and tyrosine hydroxylase (TH) expression and increased monoamine oxidase A (MAO A), glutamic acid decarboxylase (GAD) and Choline acetyltransferase (ChAT) expression. Further, naloxone altered navigational memory by decreasing the CREB and p-CREB level in hippocampus suggesting suppression of sleep inducing effect of p-DSIP. Our study demonstrates that improvement of sleep quality by p-DSIP restores spatial memory by up regulating CREB phosphorylation during simulated high altitude hypoxia.
Study Information
pubmed
2018
2018-08-11T00:00:00.000Z
10.1016/j.lfs.2018.08.026
14
61