The Effect of Peptide Semax, an ACTH(4-10) Analogue, on Intracellular Calcium Dynamics in Rat Brain Neurons.
Kolbaev. S N SN; Sharonova. I N IN; Skrebitsky. V G VG
Key Findings
- Semax (1 µM) increased the frequency of spontaneous intracellular calcium spikes in hippocampal CA1 pyramidal neurons.
- Semax did not affect proton‑induced calcium rises in cerebellar granule cells.
- The neuroprotective action of Semax likely involves mechanisms other than inhibition of acid‑sensing ion channel calcium entry.
Practical Outcomes
- For self‑experimenters, this study suggests Semax may influence hippocampal activity, but the effect is observed only in isolated rat brain tissue at micromolar concentrations. No direct dosing guidance or clear performance benefit for humans can be drawn, so it’s more of a mechanistic clue than a ready‑to‑use protocol.
Summary
In rat brain slices, the peptide Semax (at a tiny lab dose) made hippocampal neurons fire calcium signals more often, but it didn't change how cerebellar cells responded to acid. This hints that Semax’s brain‑protective effects aren't due to blocking acid‑sensing calcium channels.
Abstract
We studied the effects of Semax on spontaneous fluctuations of intracellular calcium ion concentration [Ca<sup>2+</sup>]<sub>i</sub> in pyramidal neurons on hippocampal slices and on proton-induced increase in [Ca<sup>2+</sup>]<sub>i</sub> in cerebellar granule cells in cerebellar slices. Application of Semax (1 μM), significantly increased the frequency of spontaneous [Ca<sup>2+</sup>]<sub>i</sub> fluctuations in the pyramidal layer cells of the hippocampal CA1 field, but had no significant effect on proton-stimulated increase in [Ca<sup>2+</sup>]<sub>i</sub> in cerebellar granule cells. These data provide insight into the localization of cellular targets and elucidate the dynamics of the initial stages of interaction between the peptide and the hippocampal neuronal network. The primary mechanism of the neuroprotective effect of Semax appears to be unrelated to attenuation of calcium entry through acid-sensing ion channels in cerebellar granule cells.
Study Information
pubmed
2025
2025-10-31T00:00:00.000Z
10.1007/s10517-025-06501-z
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