K. R. Uspenska, G. L. Gergalova, O. Yu. Lykhmus, M. V. Skok

Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;

e-mail: kate.uspenska@gmail.com

Mitochondrial nicotinic acetylcholine receptors (nAChRs) control permeability transition pore formation and cytochrome c release in the presence of apoptogenic factors. This study demonstrates that pharmacological agents amixin and agmatine affect mitochondrial nAChR functioning: they slightly suppress cytochrome c release from mouse brain and liver mitochondria stimulated with apoptogenic dose of Са²⁺ and prevent the effect of α7 nAChR agonist PNU282987. We conclude that mitochondria may be one of therapeutic targets of amixin and agmatine.