Modulation of GABA- and Glycine-Activated Ionic Currents with Semax in Isolated Cerebral Neurons.
Sharonova. I N IN; Bukanova. Yu V YV; Myasoedov. N F NF; Skrebitskii. V G VG
Key Findings
- Semax (1 µM) increased GABA‑activated currents in cerebellar Purkinje cells by about 147%
- Semax (0.1 µM and 1 µM) lowered glycine‑activated chloride currents in hippocampal pyramidal neurons to 68% and 43% of control
- Both effects developed slowly, were poorly reversible, and suggest involvement of second‑messenger systems
Practical Outcomes
- The results show semax can modulate inhibitory brain signals, but because the work was done in rat cells in a dish, it doesn’t give clear guidance on dosing or real‑world benefits for humans. Biohackers should treat this as early‑stage mechanistic data, not a basis for new protocols.
Summary
In a lab test on rat brain cells, the peptide semax changed how two brain chemicals work: it boosted the effect of GABA (a calming signal) and reduced the effect of glycine (another signal). These changes happened slowly and weren’t easily reversed, hinting at deeper cellular pathways, but the study was done in isolated neurons, not in living animals or people.
Abstract
The concentration-clamp experiments with neurons isolated from the rat brain showed that nootropic and neuroprotective drug Semax added to perfusion solution at concentration of 1 μM augmented the amplitude of GABA-activated ionic currents in cerebellum Purkinje cells by 147±13%. In addition, Semax in perfusion solution (0.1 and 1 μM) diminished the amplitude of glycine-activated chloride currents in hippocampal pyramidal neurons down to 68 and 43% control level, respectively. Both potentiating and inhibitory effects developed slowly, and they were poorly reversible, which indicated a probable implication of second messengers in the observed phenomena. Semax accelerated the falling edge of glycine-activated current both after a short-term co-application with agonist and after addition of this peptide into perfusion solution.
Study Information
pubmed
2018
2018-03-26T00:00:00.000Z
10.1007/s10517-018-4043-8