The study shows that the brain‑active peptide Semax can change how certain brain chemicals (acetylcholine and GABA) bind to their receptors in stressed rats. The effect depends on the dose, and Semax also appears to increase the number of GABA binding sites after stress. This suggests Semax may influence brain signaling pathways linked to memory and stress response.

An integrated methodological approach to study the molecular aspects of short regulatory neuropeptides biological mechanism is proposed. The complex research is based on radioligand-receptor method of analysis and covers such points of peptides molecular activity as: specific binding of peptides to brain cells plasmatic membranes, formation of tissue specific synacton, influence of peptides (as allosteric modulators) on functionality of different neuroreceptors as well as delayed in time effects of peptides on receptor-binding activity of well-known neuroreceptor systems. Radiolabeled ligands in such complex study are the one of the best and precision instruments to uncover the molecular mechanism of multiple and multitarget biological effects of regulatory peptides. In this issue we used heptapeptide Semax as a model regulatory peptide, [³ H]Ach and [³ H]GABA as an effector molecules, and the rat model of stress-induced memory and behavior impairment as a morbid state. We showed the ability of Semax to modulate in a dose-dependent manner [³ H]Ach and [³ H]GABA specific binding to some of its corresponding receptors as well as to affect the number of [³ H]GABA specific binding places on rat neurons plasmatic membranes after complex stress exposure.