Completed Preclinical (in vivo) 2024

    Antidepressant-like and antistress effects of Semax in rats subjected to chronic unpredictable stress

    Inozemtseva LS, Karpenko EA, Dolotov OV, et al.

    European Journal of Pharmacology

    DOI: 10.1016/j.ejphar.2024.177067

    Summary

    Demonstrated that intranasal Semax reversed chronic unpredictable stress-induced anhedonia in rats and restored hippocampal BDNF levels depleted by chronic stress. Supports Semax as a potential antidepressant agent acting through restoration of stress-depleted neurotrophic signaling.

    Key Findings

    • Semax reversed anhedonia caused by chronic unpredictable stress in rats
    • Restored hippocampal BDNF levels that were depleted by chronic stress exposure
    • Supports potential antidepressant application through neurotrophic mechanism restoration

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    Completed 2007

    Neurotrophin gene expression in rat brain under the action of Semax, an analogue of ACTH 4-10

    Agapova TY, Agniullin YV, Silachev DN, et al.

    Neuroscience Letters

    Demonstrated that Semax increases NGF and BDNF gene expression in the rat hippocampus in a region-specific manner. Effects were observed within hours of intranasal administration, supporting Semax's role as a rapid-onset modulator of neurotrophin production in the central nervous system.

    • Semax increased both NGF and BDNF gene expression in hippocampus
    • Neurotrophin upregulation was region-specific within the brain

    DOI: 10.1016/j.neulet.2007.01.029

    Completed 2006

    Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus

    Dolotov OV, Karpenko EA, Inozemtseva LS, et al.

    Brain Research

    This study investigated the effects of the synthetic heptapeptide semax (ACTH 4-10 analog, Met-Glu-His-Phe-Pro-Gly-Pro) on the expression of brain-derived neurotrophic factor (BDNF) and its receptor TrkB in the rat hippocampus. Intranasal administration of semax produced significant and sustained upregulation of BDNF mRNA and protein levels, providing a neurotrophic mechanism for its observed cognitive-enhancing effects.

    • Intranasal semax administration (50-100 mcg/kg) significantly increased BDNF mRNA expression in the rat hippocampus within 30 minutes, with effects lasting up to 24 hours
    • BDNF protein levels in the hippocampus were elevated by approximately 1.5-fold following semax treatment

    DOI: 10.1016/j.brainres.2006.06.015

    Completed 2006

    Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus

    Dolotov OV, Karpenko EA, Inozemtseva LS, et al.

    Brain Research

    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.

    • 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

    DOI: 10.1016/j.brainres.2006.09.017