It is important to note that
It is important to note that stable amnesia is, apparently, a general biological phenomenon and can be found in different animal species. In studies on rats, it was found that if reconsolidation of conditioned olfactory aversion memory was impaired by the antagonist of NMDA glutamate receptors, amnesia develops, which at the late phase (from the 10th day) is characterized by impairment of memory formation during the repeated training session . On rats trained to form spatial memory in the Morris water maze, it was revealed that the Trigonelline synthase 3 kinase inhibitor injections before the reminder caused amnesia development at a late phase and repeated training did not lead to long-term spatial memory formation . In studies on chickens, it was found that the administration of MK-801 prior to training for passive avoidance impaired memory retrieval . It is remarkable that the repeated training did not lead to memory recovery. These facts suggest that stable amnesia can be formed in the case of both consolidation and reconsolidation impairments of at least some memory types in mollusks, birds, and mammals. However, it is clear that further investigations are required to identify the specific (border) conditions for the appearance of stable amnesia in different animal species and with the usage of different training models. Mechanisms of specific impairment of long-term memory consolidation remain unclear. Stable NMDA-dependent amnesia cannot be explained by the retrieval impairment or memory trace erasure or by processes of extinction. In these cases, one would expect a memory recovery or new memory formation after the repeated training. One of the reasons for stable amnesia development might be destruction of the structural basis of memory trace. For example, this could be due to the death of neurons or elimination of synaptic connections that are functionally necessary for the maintenance of the memory [36,73,74]. However, earlier , and in the present study, it was found that during the stable amnesia in snails, the ability to form short-term memory was preserved, and therefore created the structural basis for its formation. It was also shown that in the case of memory impairment or long-term synaptic facilitation, the reduction in the number of synaptic contacts between neurons to the level registered before the training (base level) was described [36,, , ]. Previously, we  and other authors  found that the conditioned food aversion learning correlates with the facilitation of electrophysiological responses of interneurons related to defensive behaviors on the conditioned stimulus, and amnesia development after the impairment of memory reconsolidation with suppression of this facilitation. Overall, these data suggest that in the process of stable amnesia development revealed in our experiments, there was a decrease in the number of synaptic connections between neurons. However, some of the base parts of synapses were preserved and were the basis for the short-term memory formation, which was not transformed into long-term memory. One of the possible mechanisms of stable amnesia may be a modification of gene transcription, which is involved in the long-term regulation of synaptic plasticity [36,74, 76,77]. For long-term regulators of synaptic plasticity, much attention is given to the epigenetic regulators of the genome, including DNA methylation, phosphorylation, acetylation, and methylation of histones [, , , , ]. We previously demonstrated that the processes of DNA methylation can be one of the possible mechanisms for development of amnesia induced by the impairment of conditioned food aversion memory in snails . Moreover, other transcription regulation factors that contribute to long-term synaptic changes in different forms of training and in different animal species have already been identified [, , , ]. A lack of experimental data does not allow the defining of the specific role of any of the mentioned processes in the mechanism of stable amnesia.