Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus
Summary
Showed that a single intranasal application of Semax significantly upregulated BDNF protein (1.4-fold), trkB receptor phosphorylation (1.6-fold), and BDNF mRNA (3-fold) in rat hippocampus. Provides mechanistic evidence linking Semax's cognitive-enhancing effects to neurotrophin signaling.
Key Findings
- Single Semax dose increased hippocampal BDNF protein 1.4-fold and BDNF mRNA 3-fold
- TrkB receptor phosphorylation increased 1.6-fold, indicating functional neurotrophin signaling
- Mechanistically links Semax to BDNF/trkB pathway activation in the hippocampus
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