The neurotropic effects of cobalt and nickel salicylate were studied during perfusion of rat hippocampal sections with solutions of these salts at concentrations of 10-2 M, 10-3 M, 10-4 M and 10-6 M. The results of this study convincingly demonstrate that the formation of complex salts of acetylsalicylic acid with divalent metals cobalt and nickel leads to changes in neurotropic effects with varying degrees of severity. In the case of nickel salicylate, there is a decrease in the severity of the depressing neurotropic effect compared with acetylsalicylic and salicylic acids [16]. And in the case of cobalt salicylate at a concentration of 10-4 M, an activation effect is manifested. We believe that this is due to the influence of the whole complexon, since a high degree of stability is shown for cobalt salicylate, especially in an aqueous solution [10]. And this salt should remain fairly stable. In this regard, it is natural to assume that cobalt salicylate is capable of triggering other processes compared to acids and, perhaps, the mechanism of its action is less strongly associated with the COX system. The observed activation effect may be associated with a direct stimulating effect on the nerve cell and/or the result of synchronization of excitation in neural networks. It should be noted that the neurotropic effects of cobalt salicylate revealed in this work coincide in their orientation with the effect of this salt on the functioning of neurons of the subcaryngeal ganglia complex of the grape snail [10]. This indicates the uniformity of the mechanisms of influence of this salt on the nervous tissue of invertebrates and vertebrates. For nickel salicylate, only a weakening of the inhibitory effect is shown in comparison with the precursor acids, perhaps the stability constant of this salt is not high and its noticeable dissociation occurs. As a result, the released residues of acetylsalicylic acid will block COX, which will trigger a mechanism of neurotropic influence close to the effects of salt solutions, the effects of which were described earlier [16]. The contribution of nickel ions will be insignificant, because its mass fraction in the salt molecule is small. From the position of ionic mechanisms, we believe that the inhibition of the generation of total biopotentials by the studied salts is most likely associated with the suppression of the incoming sodium current. And the stimulating effect of cobalt salicylate in a concentration of 10-4 M, on the contrary, with its stimulation (relief). Also, the described effects can be realized as a result of modulation of synaptic interaction in neural networks. Elucidation of these biophysical mechanisms is a priority task of our further research. And also, the most important question remains open about the possible change in the effects of these salts with different injections of substances into the body: oral, intramuscular, intravenous, etc.