In brief
A companion to the basal-forebrain study from the same group, this time in the hippocampus. A single intranasal application of Semax at 50 micrograms per kilogram produced, at most, a 1.4-fold rise in BDNF protein together with a 1.6-fold rise in phosphorylation of its receptor trkB, and a three-fold and two-fold rise in exon III BDNF and trkB messenger RNA respectively. Treated animals also showed more conditioned avoidance reactions in a learning task. The authors propose that Semax acts on cognition by modulating the expression and activation of the hippocampal BDNF/trkB system.
Study design
Rats given a single intranasal dose of Semax; hippocampal BDNF and trkB measured, and a conditioned-avoidance task.
What it does not show
A single dose in rats with molecular endpoints and one behavioural task. The BDNF changes are modest fold-changes, and the paper does not test whether they cause the behavioural effect.
Results in rodents or other animals often do not reproduce in people. Species, route, dose and the injury or disease model all shape the outcome, and an effect in a rat is a reason for further study, not a conclusion.
Where this paper is cited
- Semax — Rat hippocampus: Semax raised BDNF and trkB expression after administration.
Other papers cited for Semax
- Animal study Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain Dolotov et al. (2006), J Neurochem
Further reading
- Research library: every paper cited on this site, by compound and by study type.
- Cognitive and longevity peptide comparison
- How to read a certificate of analysis
- Lyophilised peptide storage and stability
How this page was made: the citation was retrieved from PubMed by PMID and checked against the title on the product page; the summary was written from the paper's abstract and reports only what the abstract reports. Read the paper itself before relying on any figure here.