In earlier experiments on snails a behavioral model was empl

In earlier experiments on snails, a behavioral model was employed of certain food rejection to study the mechanisms of the reconsolidation of long-term associative memory. It was found that conditioned food stimuli (reminder) presentation, combined with injections of NMDA glutamate receptor antagonists, serotonin receptor antagonists, and protein synthesis inhibitors, 2 days after training, led to amnesia induction and facilitation suppression of electrophysiological responses in TG003 related to defensive behavior on a conditioned stimulus. This is typical for conditioned food aversion [[51], [52], [53], [54], [55]]. The administration of these substances without combining them with a reminder did not influence memory retrieval.
Results
Discussion Currently, there are several points of view on the possible mechanisms of amnesia. It is suggested that amnesia can be the consequence of memory retrieval impairment, partial or full memory trace erase [3,8, 9,[16], [17], [18]]. Possibly, during the early phase of serotonin-dependent amnesia development, there was a gradual reversion of functional and structural basics of the initial memory, which was accompanied by the impairment of its retrieval. Incomplete memory impairment at this phase can be the reason for relatively rapid formation of conditioned food aversion memory during the second training. During the late phase of serotonin-dependent amnesia, the reversion of the initial memory mechanisms were apparent, and memory erasure was completed. This assumption was confirmed by the data about the similarity of the dynamics for memory formation during the initial and the retraining during this phase of amnesia. Furthermore, in the literature, there are data obtained mainly in invertebrate animals, which allow us to discuss our results from another perspective. In particular, it was shown that the processes amnestically opposite to learning, such as forgetting or memory extinction, are active involving different neurotransmitters, intracellular signaling systems, and processes of translation and transcription [[56], [57], [58], [59], [60], [61], [62], [63]]. It can be suggested that the serotonin-dependent amnesia we studied is also active, developing in time, a process aimed at the reversal of the cellular and molecular modifications underlying memory. It should be noted that the amnesia was stable to repeated training for food aversion conditioning in snails, can also be induced after impairment of memory reconsolidation by NMDA glutamate receptor antagonist APV (DL-2-Amino-5-phosphonopentanoic acid), the antagonist of AMPA ((+) - a- amino-3-hydroxy-5-methylisoxazole-4-propionic acid hydrate) glutamate receptors DNQX (6,7-dinitroquinoxaline-2,3 (1H, 4H) -dione), and protein synthesis inhibitors, cycloheximide and anisomycine [53,64,65]. Amnesia stable to repeated training was also revealed after memory consolidation impairment using the protein synthesis inhibitor during initial training for conditioned food aversion [66]. Stable impairment of conditioned food aversion memory was identified after the administration of amnestic agents and the usage of different types of food as reminding CS. These included bananas, raw carrots, and apples [51,67]. Thus, NMDA-dependent amnesia is a specific process that manifests through an unusual behavioral phenomenon after repeated training formation of long-term aversion memory of the same type of food. This was used during the initial training as CS was impaired. In support of the hypothesis of the NMDA-dependent amnesia as the active process, there is data that was previously obtained. It was found that amnesia caused by the administration of the MK-801/reminder was suppressed by inhibitors of protein and mRNA synthesis, which were injected into snails in a certain time window (0–6 hours) after administration of the MK-801/reminder [68,69]. We hypothesized that the induction of stable amnesia is dependent on translation and transcription mechanisms.