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

@article{Dolotov2006SemaxAA,
  title={Semax, an analog of ACTH(4–10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus},
  author={Oleg V. Dolotov and E. A. Karpenko and Lyudmila S. Inozemtseva and Tamara Seredenina and Natalia G Levitskaya and Joanna Rozyczka and E. V. Dubynina and Ekaterina V. Novosadova and Lyudmila A. Andreeva and L. Yu. Alfeeva and Andrey A Kamensky and Igor A. Grivennikov and Nikolay F. Myasoedov and J{\"u}rgen Engele},
  journal={Brain Research},
  year={2006},
  volume={1117},
  pages={54-60}
}
Time course of the expression of genes of brain-derived neurotrophic factor and nerve growth factor in the hippocampus and frontal cortex induced by semax in rats
TLDR
An analysis of the time course of the expression of NGF and BDNF genes in the hippocampus and frontal cortex in rats after a single intranasal administration of semax found that semax administration resulted in a rapid long-term activation of the N GF andBDNF genes expression, which was specific for different rat brain structures investigated.
Semax and Pro-Gly-Pro Activate the Transcription of Neurotrophins and Their Receptor Genes after Cerebral Ischemia
TLDR
The analysis of the transcription alterations under PGP and Semax treatment in the cortex of rats without surgery, sham-operated rats and rats subjected to pMCAO revealed that Semax selectively affected the transcription of neurotrophins and their receptors in the ischemic rat cortex, whereas the influence of PGP was mainly unspecific.
ACTH 6-9-PGP improves memory consolidation processes in rats
TLDR
It was found that ACTH6-9-PGP had a pronounced stimulating effect on the memory consolidation process in the dose range from 0.5 μg/kg to 150 μg/ kg, which indicates the greater activity of HFRWPGP sequence in relation to memory consolidation processes and allows considering this peptide as a promising molecule for creating nootropic pharmacological drugs.
Effect of semax and its C-terminal peptide PGP on expression of neurotrophins and their receptors in rat brain during incomplete global ischemia
TLDR
The results demonstrated that ischemia caused a significant decrease in gene expression in the hippocampus, and the mechanism of Semax action was clarified and certain features of mRNA expression of neurotrophins and their receptors under experimental conditions were revealed.
Expression changes caused by the peptide semax in the intracellular signal pathway genes in rat hippocamp
TLDR
The teams from the Institute of Molecular Genetics and Moscow State University created the peptide Met–Glu– His–Phe–Pro–Gly–Pro, which was named semax, which has been shown that semax enhances the survival of brain cells during hypoxia and increases the selective attention and memory trace consolidation.
Therapeutic Possibility of “Semax” for Depression
  • C. Pae
  • Psychology, Biology
    CNS Spectrums
  • 2008
TLDR
The therapeutic possibility of a revolutionary neuropeptide, "Semax" functioning as neuroregulator, neuromodulator and neuroprotector, in relation with the treatment of major depression is suggested, indicating its potential effectiveness for elderly depressed patients who are frequently accompanied with comorbid neurological conditions.
Comparison of the Temporary Dynamics of NGF and BDNF Gene Expression in Rat Hippocampus, Frontal Cortex, and Retina Under Semax Action
TLDR
It was revealed that after Semax administration the multidirectional activation of the expression of the genes under investigation in the hippocampus, frontal cortex, and retina was observed and both neurotrophin genes was decreased in rat hippocampus and retina 20 min afterSemax administration.
The Nootropic and Analgesic Effects of Semax Given via Different Routes
TLDR
Evidence is provided that different mechanisms and brain structures are involved in mediating the nootropic and analgesic effects of Semax, and that intranasal Semax was more effective in improving learning in animals than i.p. Semax.
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References

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Semax, an analogue of adrenocorticotropin (4–10), binds specifically and increases levels of brain‐derived neurotrophic factor protein in rat basal forebrain
TLDR
Results point to the presence of specific binding sites for Semax in the rat basal forebrain, and indicate that the cognitive effects exerted by Semax might be associated, at least in part, with increased BDNF protein levels in this brain region.
N-terminal degradation of ACTH(4-10) and its synthetic analog semax by the rat blood enzymes.
Differential usage of multiple brain-derived neurotrophic factor promoters in the rat brain following neuronal activation.
TLDR
Data show that the four BDNF promoters allow multiple points ofBDNF mRNA regulation and suggest that the activation of different subtypes of glutamate receptors differentially regulates the expression of BDNF exon-specific mRNAs in the brain.
Stress and glucocorticoids affect the expression of brain-derived neurotrophic factor and neurotrophin-3 mRNAs in the hippocampus
TLDR
It is demonstrated that BDNF and NT-3 are stress-responsive genes and the possibility that alterations in the expression of these or other growth factors might be important in producing some of the physiological and pathophysiological effects of stress in the hippocampus is raised.
SYNTHETIC ACTH ANALOGUE SEMAX DISPLAYS NOOTROPIC-LIKE ACTIVITY IN HUMANS
SUMMARY Nootropic properties of ACTH4-10 analogue, Semax, were demonstrated in experiments with human volunteers. The antihypoxic effect of Semax was shown by EEG analysis after shortterm
Differential effects of melanocortin peptides on neural melanocortin receptors.
TLDR
Analysis of the structure-activity relationships (SARs) of peptides derived from adrenocorticotropic hormone with cloned MC3 and MC4 receptors in vitro and correlated these with central effects of MCs in vivo identifies peptides with selectivity for either the MC3 receptor or the MC4 receptor, which may be used for development of novel MC receptor-specific ligands.
BDNF Up‐Regulates TrkB Protein and Prevents the Death of CA1 Neurons Following Transient Forebrain Ischemia
TLDR
Grafting of BDNF‐producing fibroblasts two days before ischemia significantly and specifically prevented nerve cells from dying in the CA1 area of the ipsilateral hippocampus and showed that BDNF is able to up‐regulate the expression of TrkB in control and pathological states.
Regional brain-derived neurotrophic factor mRNA and protein levels following transient forebrain ischemia in the rat.
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