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Head-to-Head Comparison: HPA Axis Biology
Both Selank and DSIP normalise HPA axis hyperactivity in CUS models, but through distinct mechanisms: Selank CUS 14 days (50 µg/kg/day i.n.): Corticosterone AUC −36% (480 → 308 nmol/L peak); GR hippocampus mRNA 84% of naive; DST: post-DEX suppression 28 nmol/L
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- Both Selank and DSIP normalise HPA axis hyperactivity in CUS models, but through distinct mechanisms:
- Selank CUS 14 days (50 µg/kg/day i.n.): Corticosterone AUC −36% (480 → 308 nmol/L peak); GR hippocampus mRNA 84% of naive; DST: post-DEX suppression 28 nmol/L (vehicle 84 nmol/L — CUS resistance reversed, approaching naive suppression ≤15 nmol/L); DRN 5-HT2C sensitivity restoration (DOI head twitch −28–34%).
- DSIP CUS 14 days (25 µg/kg/day i.c.v.): Corticosterone AUC −22–28% (more modest overall reduction); diurnal amplitude: AM/PM ratio +28–34% (rhythmicity restored more than absolute suppression); ACTH pulsatility: 3.2 → 4.6 pulses/3h (pattern normalisation); SWS 18 → 32% (sleep architecture improvement secondary to HPA normalisation — bidirectional relationship).
- Key distinction: Selank suppresses cortisol output and restores GR sensitivity — targeting the effector arm of HPA dysregulation. DSIP restores the temporal patterning of ACTH pulsatility and diurnal amplitude — targeting the rhythmic architecture of HPA regulation. In research designs studying whether total glucocorticoid load drives pathology (Selank preferred) versus whether disrupted circadian HPA patterning is the pathological variable (DSIP preferred), agent selection is mechanistically determinative.