By protein engeneering of ammodytoxin, a presynaptically neurotoxic phospholipase A2, we determined the first two areas on the molecule of the toxin, which are responsible for its neurotoxicity. In 2001 we published the discovery of two ammodytoxin receptors in cerebral cortx, the new, neuronal form of the M-type phospholipase A2 receptor in plasma membrane and calmodulin in the cytosol of the nerve cell. We proposed a hypothesis about the mechanism of action of presynaptically acting phospholipases A2. We suggested that, following the association with a specific receptor in axolemma and internalisation, a phospholipase A2 neurotoxin exerts its action intracellularly. In 2002 we defined additional elements on the molecule of ammodytoxin responsible for its high neurotoxicity. The low yield expression of some ammodytoxin mutants was explained by the analysis of their mRNA secundary structures. In the year 2003 we described two novel intracellular ammodytoxin-binding proteins, gamma and epsilon isoforms of 14-3-3 protein. We mapped also a calmodulin-binding site on the surface of ammodytoxin, which seems to be non-conventional. In collaboration with G. Faure, Institut Pasteur, Paris we studied and compared the action of ammodytoxin-related dimeric neurotoxic phospholipase A2, crotoxin. We published the characterisation of a brain acceptor for crotoxin in Toxicon 41 (2003) 509-517. In 1999 we published the first work about the evolution of retrotransposons in vertebrates and in 2000 the work on accelerated or adaptive evolution. We studied the evolution of a proteinase inhibitor in Vipera a. ammodytes venom and established the adaptive evolution also in this case. In addition, we studied the dinamics of evolution and the distribution of retrotransposons. Neurotoxic phospholipases A2 from different snake venoms are subject of extensive research in many countries. Inspite of the fact that these toxins bind to different targets in neurons, final effects of their actions sre almost identical. Several groups worldwide is trying to explain their patological action on the molecular level. Our group is one of the most experienced groups on receptors for neurotoxic phospholipases A2 and we hope to be the first to unveil the molecular basis of action of these molecules on nerve cells. This result is of a general scientific importance as it may open the way to develop new diagnostics and drugs. (European Biotechnology News (2003) Vol.2, No. 4 p.20 called attention to our achievement. Copy is attached).